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Dr. Noha Elemam
University of Sharjah

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0 Autoimmune Diseases
0 Cancer
0 Immunology
0 MicroRNAs
0 Immuno-oncology

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Natural Killer Cells
MicroRNAs
Cancer
Autoimmune Diseases

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Review
Published: 07 June 2021 in Journal of Immunology Research
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Natural killer cells (NK cells) are a crucial constituent of the innate immune system as they mediate immunity against viruses, bacteria, parasites, and most importantly, tumor cells. The exact mechanism of how the innate immune system and specifically NK cells interact with cancer cells is complex and is yet to be understood. Several factors that constitute the tumor microenvironment (TME) such as hypoxia and TGF-β are believed to play a role in the complex physiological reaction of NK cells to tumor cells. On the other hand, several risk factors are implicated in the development and progression of breast cancer, most importantly: obesity. Cytokines released from adipose tissue such as adipokines, leptin, and resistin, among others, are also believed to facilitate tumor progression. In this study, we aimed to build a triad of breast cancer, obesity, and NK cell dysfunction to elucidate a link between these pillars on a cellular level. Directing efforts towards solidifying the link between these factors will help in designing a targeted immunotherapy with a low side-effect profile that can revolutionize breast cancer treatment and improve survival in obese patients.

ACS Style

Esraa Elaraby; Abdullah Imadeddin Malek; Hanan W. Abdullah; Noha Mousaad Elemam; Maha Saber-Ayad; Iman M. Talaat. Natural Killer Cell Dysfunction in Obese Patients with Breast Cancer: A Review of a Triad and Its Implications. Journal of Immunology Research 2021, 2021, 1 -10.

AMA Style

Esraa Elaraby, Abdullah Imadeddin Malek, Hanan W. Abdullah, Noha Mousaad Elemam, Maha Saber-Ayad, Iman M. Talaat. Natural Killer Cell Dysfunction in Obese Patients with Breast Cancer: A Review of a Triad and Its Implications. Journal of Immunology Research. 2021; 2021 ():1-10.

Chicago/Turabian Style

Esraa Elaraby; Abdullah Imadeddin Malek; Hanan W. Abdullah; Noha Mousaad Elemam; Maha Saber-Ayad; Iman M. Talaat. 2021. "Natural Killer Cell Dysfunction in Obese Patients with Breast Cancer: A Review of a Triad and Its Implications." Journal of Immunology Research 2021, no. : 1-10.

Original research
Published: 01 June 2021 in Journal of Inflammation Research
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Objective: Herceptin (trastuzumab) is an approved drug for treating HER2+ breast cancer patients, but its use for other diseases is not established. We sought to investigate the effects of Herceptin on ameliorating experimental autoimmune encephalomyelitis (EAE) and to examine its effects on the expression of various genes. Methods: We used in-silico analysis of publicly available data, qRT-PCR, and immunohistochemistry (IHC) to determine the expression of HER2+ cells in the brains of EAE mice. IHC was also utilized to determine the anti-inflammatory effects of Herceptin. The ability of Herceptin to alleviate the EAE clinical score was measured in these mice. Bioinformatics analysis of publicly available data and qRT-PCR were performed to investigate the differentially expressed genes that were either up-regulated or down-regulated during the high clinical score (HCS) of the disease. Results: We observed that HER2/Erbb2, the receptor for Herceptin is upregulated in the brains of EAE mice when the brains were examined at the HCS stage. Further, we demonstrated that Herceptin ameliorates the EAE disease, increasing re-myelination, reducing brain inflammation, CD3+ T cell accumulation, and HER2+ cells in the brains of these mice. Molecular analysis demonstrated the expression of different genes that were either up-regulated or down-regulated during the HCS of the disease. Our combined bioinformatics and qRT-PCR analyses show increased mRNA expression of Atp6v0d2, C3, C3ar1, Ccl3, Ccl6, Cd74, Clec7a, Cybb, H2-Aa, Hspb1, Lilr4b, Lilrb4a, Mpeg1, Ms4a4a, Ms4a6c, Saa3, Serpina3n and Timp1, at HCS. Except for the mRNA levels of Cd74 and Clec7a which were increased at HCS when Herceptin was used in both prophylactic and therapeutic regimens, the levels of other described mRNAs were reduced. Conclusion: These novel findings show that Herceptin ameliorates the clinical score in EAE mice and are the first to investigate in detail the differential gene expression post-treatment with the drug.

ACS Style

Mena Al-Ani; Noha Mousaad Elemam; Ibrahim Y Hachim; Tom K Raju; Jibran Sualeh Muhammad; Mahmood Y Hachim; Riyad Bendardaf; Azzam A Maghazachi. Molecular Examination of Differentially Expressed Genes in the Brains of Experimental Autoimmune Encephalomyelitis Mice Post Herceptin Treatment. Journal of Inflammation Research 2021, ume 14, 2601 -2617.

AMA Style

Mena Al-Ani, Noha Mousaad Elemam, Ibrahim Y Hachim, Tom K Raju, Jibran Sualeh Muhammad, Mahmood Y Hachim, Riyad Bendardaf, Azzam A Maghazachi. Molecular Examination of Differentially Expressed Genes in the Brains of Experimental Autoimmune Encephalomyelitis Mice Post Herceptin Treatment. Journal of Inflammation Research. 2021; ume 14 ():2601-2617.

Chicago/Turabian Style

Mena Al-Ani; Noha Mousaad Elemam; Ibrahim Y Hachim; Tom K Raju; Jibran Sualeh Muhammad; Mahmood Y Hachim; Riyad Bendardaf; Azzam A Maghazachi. 2021. "Molecular Examination of Differentially Expressed Genes in the Brains of Experimental Autoimmune Encephalomyelitis Mice Post Herceptin Treatment." Journal of Inflammation Research ume 14, no. : 2601-2617.

Journal article
Published: 17 May 2021 in International Journal of Molecular Sciences
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The global coronavirus disease 2019 (COVID-19) pandemic was associated with multiple organ failure and comorbidities, such as type 2 diabetes mellitus (T2DM). Risk factors, such as age, gender, and obesity, were associated with COVID-19 infection. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is known to use several host receptors for viral entry, such as angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) in the lung and other organs. However, ACE2 could be shed from the surface to be soluble ACE2 (sACE2) in the circulation. The epigenetic factors affecting ACE2 expression include a type of small non-coding RNAs called microRNAs (miRNAs). In this study, we aimed at exploring the status of the sACE2 as well as serum levels of several upstream novel miRNAs as non-invasive biomarkers that might have a potential role in T2DM patients. Serum samples were collected from 50 T2DM patients and 50 healthy controls, and sACE2 levels were quantified using enzyme-linked immunosorbent assay (ELISA). Also, RNA was extracted, and TaqMan miRNA reverse transcription quantitative PCR (RT-qPCR) was performed to measure serum miRNA levels. Our results revealed that sACE2 is decreased in the T2DM patients and is affected by age, gender, and obesity level. Additionally, 4 miRNAs, which are revealed by in silico analysis to be potentially upstream of ACE2 were detectable in the serum. Among them, miR-421 level was found to be decreased in the serum of diabetic patients, regardless of the presence or absence of diabetic complications, as well as being differential in various body mass index (BMI) groups. The other 3 miRNAs (miR-3909, miR-212-5p, and miR-4677-3p) showed associations with multiple factors including age, gender, BMI, and serum markers, in addition to being correlated to each other. In conclusion, our study reveals a decline in the circulating serum levels of sACE2 in T2DM patients and identified 4 novel miRNAs that were associated with T2DM, which are influenced by different clinical and demographic factors.

ACS Style

Noha Elemam; Hind Hasswan; Hayat Aljaibeji; Nabil Sulaiman. Circulating Soluble ACE2 and Upstream microRNA Expressions in Serum of Type 2 Diabetes Mellitus Patients. International Journal of Molecular Sciences 2021, 22, 5263 .

AMA Style

Noha Elemam, Hind Hasswan, Hayat Aljaibeji, Nabil Sulaiman. Circulating Soluble ACE2 and Upstream microRNA Expressions in Serum of Type 2 Diabetes Mellitus Patients. International Journal of Molecular Sciences. 2021; 22 (10):5263.

Chicago/Turabian Style

Noha Elemam; Hind Hasswan; Hayat Aljaibeji; Nabil Sulaiman. 2021. "Circulating Soluble ACE2 and Upstream microRNA Expressions in Serum of Type 2 Diabetes Mellitus Patients." International Journal of Molecular Sciences 22, no. 10: 5263.

Covid 19
Published: 08 April 2021 in Current Medical Research and Opinion
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In March 2020, COVID-19 infection caused by SARS-CoV-2 has been declared to be a global pandemic, where its complications, severity and mortality are reported to be due to the released inflammatory cytokines or the so-called cytokine storm. This is quite similar to that observed in the autoimmune and chronic inflammatory rheumatic disease, rheumatoid arthritis (RA). It was hypothesized that RA patients are at a higher risk of acquiring COVID-19; however, recent studies reported that they are not when compared to the rest of the population. In this review, we aim to highlight the mutual pathological features, cytokine profiles and risk factors between COVID-19 and RA. Also, many researchers are currently working to explore therapeutic agents that could aid in the eradication of COVID-19 infection. Due to the similarity between the inflammation status in COVID-19 and RA, many anti-rheumatic drugs such as hydroxychloroquine, tocilizumab, baricitinib and anakinra were proposed to be therapeutic modalities for COVID-19 infection.

ACS Style

Noha Mousaad Elemam; Azzam A. Maghazachi; Suad Hannawi. COVID-19 infection and rheumatoid arthritis: mutual outburst cytokines and remedies. Current Medical Research and Opinion 2021, 37, 929 -938.

AMA Style

Noha Mousaad Elemam, Azzam A. Maghazachi, Suad Hannawi. COVID-19 infection and rheumatoid arthritis: mutual outburst cytokines and remedies. Current Medical Research and Opinion. 2021; 37 (6):929-938.

Chicago/Turabian Style

Noha Mousaad Elemam; Azzam A. Maghazachi; Suad Hannawi. 2021. "COVID-19 infection and rheumatoid arthritis: mutual outburst cytokines and remedies." Current Medical Research and Opinion 37, no. 6: 929-938.

Review
Published: 01 February 2021 in Sci
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Multiple sclerosis (MS) is a chronic autoimmune disease that affects the myelination of the neurons present in the central nervous system (CNS). The exact etiology of MS development is unclear, but various environmental and genetic factors might play a role in initiating the disease. Experimental autoimmune encephalomyelitis (EAE) is a mouse model that is used to study the pathophysiology of MS disease as well as the effects of possible therapeutic agents. In addition, autoreactive immune cells trigger an inflammatory process upon the recognition of CNS antigens, which leads to destruction of the neurons. These include innate immune cells such as macrophages, dendritic cells, and natural killer cells. Additionally, the activation and extravasation of adaptive immune cells such as CD4+ T cells into the CNS may lead to further exacerbation of the disease. However, many studies revealed that immune cells could have either a protective or pathological role in MS. In this review, we highlight the roles of innate and adaptive immune cellular and soluble players that contribute to the pathogenesis of MS and EAE, which may be used as potential targets for therapy.

ACS Style

Sarah Dhaiban; Mena Al-Ani; Noha Elemam; Mahmood Al-Aawad; Zeinab Al-Rawi; Azzam Maghazachi. Role of Peripheral Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. Sci 2021, 3, 12 .

AMA Style

Sarah Dhaiban, Mena Al-Ani, Noha Elemam, Mahmood Al-Aawad, Zeinab Al-Rawi, Azzam Maghazachi. Role of Peripheral Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. Sci. 2021; 3 (1):12.

Chicago/Turabian Style

Sarah Dhaiban; Mena Al-Ani; Noha Elemam; Mahmood Al-Aawad; Zeinab Al-Rawi; Azzam Maghazachi. 2021. "Role of Peripheral Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis." Sci 3, no. 1: 12.

Preprint
Published: 18 November 2020
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Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS) characterized by varying degrees of demyelination of uncertain etiology, and is associated with specific environmental and genetic factors. Upon recognition of CNS antigens, the immune cells initiate an inflammatory process which leads to destruction and deterioration of the neurons. Innate immune cells such as macrophages, dendritic cells and natural killer cells are known to play critical roles in the pathogenesis of MS. Also, the activation of peripheral CD4+ T cells by CNS antigens leads to their extravasation into the CNS causing damages that exacerbates the disease. This could be accompanied by dysregulation of T regulatory cells and other cell types functions. Experimental autoimmune encephalomyelitis (EAE) is a mouse model used to study the pathophysiology of MS disease. In this review, we highlight the roles of innate and adaptive immune players in the pathogenesis of MS and EAE.

ACS Style

Sarah Dhaiban; Mena Al-Ani; Noha Mousaad Elemam; Mahmood H Al-Aawad; Zeinab Al-Rawi; Azzam A. Maghazachi. Role of Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. 2020, 1 .

AMA Style

Sarah Dhaiban, Mena Al-Ani, Noha Mousaad Elemam, Mahmood H Al-Aawad, Zeinab Al-Rawi, Azzam A. Maghazachi. Role of Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. . 2020; ():1.

Chicago/Turabian Style

Sarah Dhaiban; Mena Al-Ani; Noha Mousaad Elemam; Mahmood H Al-Aawad; Zeinab Al-Rawi; Azzam A. Maghazachi. 2020. "Role of Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis." , no. : 1.

Review
Published: 01 September 2020 in Infection and Drug Resistance
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COVID-19 infection caused by the newly discovered coronavirus severe acute respiratory distress syndrome virus-19 (SARS-CoV-2) has become a pandemic issue across the globe. There are currently many investigations taking place to look for specific, safe and potent anti-viral agents. Upon transmission and entry into the human body, SARS-CoV-2 triggers multiple immune players to be involved in the fight against the viral infection. Amongst these immune cells are NK cells that possess robust antiviral activity, and which do not require prior sensitization. However, NK cell count and activity were found to be impaired in COVID-19 patients and hence, could become a potential therapeutic target for COVID-19. Several drugs, including glatiramer acetate (GA), vitamin D3, dimethyl fumarate (DMF), monomethyl fumarate (MMF), natalizumab, ocrelizumab, and IFN-β, among others have been previously described to increase the biological activities of NK cells especially their cytolytic potential as reported by upregulation of CD107a, and the release of perforin and granzymes. In this review, we propose that such drugs could potentially restore NK cell activity allowing individuals to be more protective against COVID-19 infection and its complications.

ACS Style

Mena Al-Ani; Noha Mousaad Elemam; Jennifer Elisabeth Hundt; Azzam A Maghazachi. Drugs for Multiple Sclerosis Activate Natural Killer Cells: Do They Protect Against COVID-19 Infection? Infection and Drug Resistance 2020, ume 13, 3243 -3254.

AMA Style

Mena Al-Ani, Noha Mousaad Elemam, Jennifer Elisabeth Hundt, Azzam A Maghazachi. Drugs for Multiple Sclerosis Activate Natural Killer Cells: Do They Protect Against COVID-19 Infection? Infection and Drug Resistance. 2020; ume 13 ():3243-3254.

Chicago/Turabian Style

Mena Al-Ani; Noha Mousaad Elemam; Jennifer Elisabeth Hundt; Azzam A Maghazachi. 2020. "Drugs for Multiple Sclerosis Activate Natural Killer Cells: Do They Protect Against COVID-19 Infection?" Infection and Drug Resistance ume 13, no. : 3243-3254.

Review
Published: 01 September 2020 in Journal of Inflammation Research
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Multiple sclerosis (MS) is an immune-mediated and neurodegenerative disorder that results in inflammation and demyelination of the central nervous system (CNS). MS symptoms include walking difficulties, visual weakening, as well as learning and memory impairment, thus affecting the quality of the patient’s life. Chemokines and chemokine receptors are expressed on the immune cells as well as the CNS resident cells. Several sets of chemokine receptors and their ligands tend to be pathogenic players in MS, including CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL17, CCL19, CCL21, CCL22, CXCL1, CXCL8, CXCL9, CXCL10, CXCL11, and CXCL16. Furthermore, current modulatory drugs that are used in the treatment of MS and its animal model, the experimental autoimmune encephalomyelitis (EAE), affect the expression of several chemokine and chemokine receptors. In this review, we highlight the pathogenic roles of chemokines and their receptors as well as utilizing them as potential therapeutic targets through selective agents, such as specific antibodies and receptor blockers, or indirectly through MS or EAE immunomodulatory drugs.

ACS Style

Sarah Dhaiban; Mena Al-Ani; Noha Mousaad Elemam; Azzam A Maghazachi. Targeting Chemokines and Chemokine Receptors in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. Journal of Inflammation Research 2020, ume 13, 619 -633.

AMA Style

Sarah Dhaiban, Mena Al-Ani, Noha Mousaad Elemam, Azzam A Maghazachi. Targeting Chemokines and Chemokine Receptors in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis. Journal of Inflammation Research. 2020; ume 13 ():619-633.

Chicago/Turabian Style

Sarah Dhaiban; Mena Al-Ani; Noha Mousaad Elemam; Azzam A Maghazachi. 2020. "Targeting Chemokines and Chemokine Receptors in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis." Journal of Inflammation Research ume 13, no. : 619-633.

Review
Published: 09 August 2020 in Cancers
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The innate immune system is the first line of defense against invading pathogens and has a major role in clearing transformed cells, besides its essential role in activating the adaptive immune system. Macrophages, dendritic cells, NK cells, and granulocytes are part of the innate immune system that accumulate in the tumor microenvironment such as breast cancer. These cells induce inflammation in situ by secreting cytokines and chemokines that promote tumor growth and progression, in addition to orchestrating the activities of other immune cells. In breast cancer microenvironment, innate immune cells are skewed towards immunosuppression that may lead to tumor evasion. However, the mechanisms by which immune cells could interact with breast cancer cells are complex and not fully understood. Therefore, the importance of the mammary tumor microenvironment in the development, growth, and progression of cancer is widely recognized. With the advances of using bioinformatics and analyzing data from gene banks, several genes involved in NK cells of breast cancer individuals have been identified. In this review, we discuss the activities of certain genes involved in the cross-talk among NK cells and breast cancer. Consequently, altering tumor immune microenvironment can make breast tumors more responsive to immunotherapy.

ACS Style

Israa Shihab; Bariaa A. Khalil; Noha Mousaad Elemam; Ibrahim Y. Hachim; Mahmood Yaseen Hachim; Rifat A. Hamoudi; Azzam A. Maghazachi. Understanding the Role of Innate Immune Cells and Identifying Genes in Breast Cancer Microenvironment. Cancers 2020, 12, 2226 .

AMA Style

Israa Shihab, Bariaa A. Khalil, Noha Mousaad Elemam, Ibrahim Y. Hachim, Mahmood Yaseen Hachim, Rifat A. Hamoudi, Azzam A. Maghazachi. Understanding the Role of Innate Immune Cells and Identifying Genes in Breast Cancer Microenvironment. Cancers. 2020; 12 (8):2226.

Chicago/Turabian Style

Israa Shihab; Bariaa A. Khalil; Noha Mousaad Elemam; Ibrahim Y. Hachim; Mahmood Yaseen Hachim; Rifat A. Hamoudi; Azzam A. Maghazachi. 2020. "Understanding the Role of Innate Immune Cells and Identifying Genes in Breast Cancer Microenvironment." Cancers 12, no. 8: 2226.

Journal article
Published: 30 April 2020 in Genes
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Rheumatoid arthritis (RA) is one of the most prevalent autoimmune diseases, while its molecular triggers are not fully understood. A few studies have shown that natural killer (NK) cells may play either a pathogenic or a protective role in RA. In this study, we sought to explore NK cell markers that could be plausibly used in evaluating the differences among healthy controls and RA patients. Publicly available transcriptome datasets from RA patients and healthy volunteers were analyzed, in order to identify differentially expressed genes (DEGs) between 1. different immune cells as compared to NK cells, and 2. NK cells of RA patients and healthy controls. The identified DEGs were validated using 16 healthy controls and 17 RA patients. Peripheral blood mononuclear cells (PBMCs) were separated by Ficoll density gradient method, while NK cells were isolated using RosetteSep technique. RNA was extracted and gene expression was assessed using RT-qPCR. All selected genes were differentially expressed in NK cells compared to PBMCs. CD56, CXCL16, PECAM-1, ITGB7, BTK, TLR10, and IL-1β were significantly upregulated, while CCL2, CCR4, RELA and IBTK were downregulated in the NK cells of RA patients when compared to healthy controls. Therefore, these NK specific genes might be used as promising biomarkers for RA diagnosis.

ACS Style

Noha Mousaad Elemam; Mahmood Yaseen Hachim; Suad Hannawi; Azzam A. Maghazachi. Differentially Expressed Genes of Natural Killer Cells Can Distinguish Rheumatoid Arthritis Patients from Healthy Controls. Genes 2020, 11, 492 .

AMA Style

Noha Mousaad Elemam, Mahmood Yaseen Hachim, Suad Hannawi, Azzam A. Maghazachi. Differentially Expressed Genes of Natural Killer Cells Can Distinguish Rheumatoid Arthritis Patients from Healthy Controls. Genes. 2020; 11 (5):492.

Chicago/Turabian Style

Noha Mousaad Elemam; Mahmood Yaseen Hachim; Suad Hannawi; Azzam A. Maghazachi. 2020. "Differentially Expressed Genes of Natural Killer Cells Can Distinguish Rheumatoid Arthritis Patients from Healthy Controls." Genes 11, no. 5: 492.

Journal article
Published: 23 April 2020 in Genes
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The United Arab Emirates National Diabetes and Lifestyle Study (UAEDIAB) has identified obesity, hypertension, obstructive sleep apnea, and dyslipidemia as common phenotypic characteristics correlated with diabetes mellitus status. As these phenotypes are usually linked with genetic variants, we hypothesized that these phenotypes share single nucleotide polymorphism (SNP)-clusters that can be used to identify causal genes for diabetes. We explored the National Human Genome Research Institute-European Bioinformatics Institute Catalog of Published Genome-Wide Association Studies (NHGRI-EBI GWAS) to list SNPs with documented association with the UAEDIAB-phenotypes as well as diabetes. The shared chromosomal regions affected by SNPs were identified, intersected, and searched for Enriched Ontology Clustering. The potential SNP-clusters were validated using targeted DNA next-generation sequencing (NGS) in two Emirati diabetic patients. RNA sequencing from human pancreatic islets was used to study the expression of identified genes in diabetic and non-diabetic donors. Eight chromosomal regions containing 46 SNPs were identified in at least four out of the five UAEDIAB-phenotypes. A list of 34 genes was shown to be affected by those SNPs. Targeted NGS from two Emirati patients confirmed that the identified genes have similar SNP-clusters. ASAH1, LRP4, FES, and HSD17B12 genes showed the highest SNPs rate among the identified genes. RNA-seq analysis revealed high expression levels of HSD17B12 in human islets and to be upregulated in type 2 diabetes (T2D) donors. Our integrative phenotype-genotype approach is a novel, simple, and powerful tool to identify clinically relevant potential biomarkers in diabetes. HSD17B12 is a novel candidate gene for pancreatic β-cell function.

ACS Style

Mahmood Y. Hachim; Hayat Aljaibeji; Rifat A. Hamoudi; Ibrahim Y. Hachim; Noha M. Elemam; Abdul Khader Mohammed; Albert Salehi; Jalal Taneera; Nabil Sulaiman. An Integrative Phenotype–Genotype Approach Using Phenotypic Characteristics from the UAE National Diabetes Study Identifies HSD17B12 as a Candidate Gene for Obesity and Type 2 Diabetes. Genes 2020, 11, 461 .

AMA Style

Mahmood Y. Hachim, Hayat Aljaibeji, Rifat A. Hamoudi, Ibrahim Y. Hachim, Noha M. Elemam, Abdul Khader Mohammed, Albert Salehi, Jalal Taneera, Nabil Sulaiman. An Integrative Phenotype–Genotype Approach Using Phenotypic Characteristics from the UAE National Diabetes Study Identifies HSD17B12 as a Candidate Gene for Obesity and Type 2 Diabetes. Genes. 2020; 11 (4):461.

Chicago/Turabian Style

Mahmood Y. Hachim; Hayat Aljaibeji; Rifat A. Hamoudi; Ibrahim Y. Hachim; Noha M. Elemam; Abdul Khader Mohammed; Albert Salehi; Jalal Taneera; Nabil Sulaiman. 2020. "An Integrative Phenotype–Genotype Approach Using Phenotypic Characteristics from the UAE National Diabetes Study Identifies HSD17B12 as a Candidate Gene for Obesity and Type 2 Diabetes." Genes 11, no. 4: 461.

Original research
Published: 01 March 2020 in Journal of Inflammation Research
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Objective: To investigate, in detail, the effects of rituximab (RTX), an off-label drug for treating multiple sclerosis (MS) disease on preventing and/or ameliorating experimental autoimmune encephalomyelitis (EAE). Methods: Using bioinformatics analysis of publicly available transcriptomics data, we determined the accumulation of B cells, plasma cells and T cells in different compartments of multiple sclerosis patients (MS) and healthy individual brains. Based on these observations and on the literature search, we dosed RTX in EAE mice either orally, or injected intraperitoneally (IP). The latter route was used either prophylactically (asymptomatic stage; upon the induction of the disease), or therapeutically (acute stage; upon the appearance of the first sign of the disease). Further, we used RTX as a preventive drug either as a single agent or in combination with other routes of administration. Results: Because no complete recovery was observed when RTX was used prophylactically or therapeutically, we devised another protocol of injecting this drug before the onset of the disease and designated this regiment as prevention. We demonstrated that the 20 μg/mouse prevention completely reduced the EAE clinical score, impaired infiltration of T and B cells into the perivascular space of mice brains, along with inhibiting the inflammation and demyelination. However, the 5 and 10 μg/mouse doses although reduced all aspects of inflammation in these mice, their effects were not as potent as the 20 μg/mouse RTX dose. Finally, we combined the 5 μg/mouse prevention treatment with either the prophylactic or therapeutic regimen and observed a robust effect. Conclusion: We observed that combinatorial regimens resulted in further reduction of inflammation, T and B cell extravasation into the brains of EAE mice and improved the re-myelination.

ACS Style

Mena R Al-Ani; Tom K Raju; Mahmood Y Hachim; Ibrahim Y Hachim; Noha M Elemam; Maha Guimei; Riyad Bendardaf; Azzam A Maghazachi. Rituximab Prevents the Development of Experimental Autoimmune Encephalomyelitis (EAE): Comparison with Prophylactic, Therapeutic or Combinational Regimens. Journal of Inflammation Research 2020, ume 13, 151 -164.

AMA Style

Mena R Al-Ani, Tom K Raju, Mahmood Y Hachim, Ibrahim Y Hachim, Noha M Elemam, Maha Guimei, Riyad Bendardaf, Azzam A Maghazachi. Rituximab Prevents the Development of Experimental Autoimmune Encephalomyelitis (EAE): Comparison with Prophylactic, Therapeutic or Combinational Regimens. Journal of Inflammation Research. 2020; ume 13 ():151-164.

Chicago/Turabian Style

Mena R Al-Ani; Tom K Raju; Mahmood Y Hachim; Ibrahim Y Hachim; Noha M Elemam; Maha Guimei; Riyad Bendardaf; Azzam A Maghazachi. 2020. "Rituximab Prevents the Development of Experimental Autoimmune Encephalomyelitis (EAE): Comparison with Prophylactic, Therapeutic or Combinational Regimens." Journal of Inflammation Research ume 13, no. : 151-164.

Review
Published: 01 March 2020 in ImmunoTargets and Therapy
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Rheumatoid arthritis (RA) is one of the most prevalent autoimmune diseases and a prototypic inflammatory disease, affecting the small joints of the hands and feet. Chemokines and chemokine receptors play a critical role in RA pathogenesis via immune cells recruitment. Several chemokines and chemokine receptors are abundant in the peripheral blood and in the local inflamed joints of RA. Furthermore, synthetic and biologics disease modifying anti rheumatic drugs have been reported to affect chemokines expression. Thus, many studies have focused on targeting chemokines and chemokine receptors, where some have shown positive promising results. However, most of the chemokine blockers in human trials of RA treatment displayed some failures that can be attributed to several reasons in their structures and binding affinities. Nevertheless, targeting chemokines will continue to be under development, in order to improve their therapeutic potentials in RA and other autoimmune diseases. In this review we provide an up-to-date knowledge regarding the role of chemokines and chemokine receptors in RA with an emphasis on their activities on immune cells. We also discussed the effects of drugs targeting those molecules in RA. This knowledge might provide impetus for developing new therapeutic modalities to treat this chronic disease.

ACS Style

Noha Mousaad Elemam; Suad Hannawi; Azzam A Maghazachi. Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis. ImmunoTargets and Therapy 2020, ume 9, 43 -56.

AMA Style

Noha Mousaad Elemam, Suad Hannawi, Azzam A Maghazachi. Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis. ImmunoTargets and Therapy. 2020; ume 9 ():43-56.

Chicago/Turabian Style

Noha Mousaad Elemam; Suad Hannawi; Azzam A Maghazachi. 2020. "Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis." ImmunoTargets and Therapy ume 9, no. : 43-56.

Slb member insight review
Published: 21 February 2020 in Journal of Leukocyte Biology
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Pyroptosis is a newly discovered programmed cell death with inflammasome formation. Pattern recognition receptors that identify repetitive motifs of prospective pathogens such as LPS of gram‐negative bacteria are crucial to pyroptosis. Upon stimulation by pathogen‐associated molecular patterns or damage‐associated molecular patterns, proinflammatory cytokines, mainly IL‐1 family members IL‐1β and IL‐18, are released through pyroptosis specific pore‐forming protein, gasdermin D. Even though IL‐1 family members are mainly involved in innate immunity, they can be factors in adaptive immunity. Given the importance of IL‐1 family members in health and diseases, deciphering the role of pyroptosis in the regulation of innate and adaptive immunity is of great importance, especially with the recent progress in identifying the exact mechanism of such a pathway. In this review, we will focus on how the innate inflammatory mediators can regulate the adaptive immune system and vice versa via pyroptosis.

ACS Style

Mahmood Hachim; Bariaa A. Khalil; Noha Mousaad Elemam; Azzam A. Maghazachi. Pyroptosis: The missing puzzle among innate and adaptive immunity crosstalk. Journal of Leukocyte Biology 2020, 108, 323 -338.

AMA Style

Mahmood Hachim, Bariaa A. Khalil, Noha Mousaad Elemam, Azzam A. Maghazachi. Pyroptosis: The missing puzzle among innate and adaptive immunity crosstalk. Journal of Leukocyte Biology. 2020; 108 (1):323-338.

Chicago/Turabian Style

Mahmood Hachim; Bariaa A. Khalil; Noha Mousaad Elemam; Azzam A. Maghazachi. 2020. "Pyroptosis: The missing puzzle among innate and adaptive immunity crosstalk." Journal of Leukocyte Biology 108, no. 1: 323-338.

Original research
Published: 01 January 2020 in Journal of Asthma and Allergy
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Introduction: The proper use of serum periostin (POSTN) as a biomarker for asthma is hindered by inconsistent performance in different clinical settings. Objective: To explore patient’s factors that may affect POSTN expression locally and systematically and its utility as a biomarker for asthma development. Materials and Methods: Here we used bioinformatics analysis of publicly available transcriptomics data to confirm that POSTN is an asthma specific gene involved in core signaling pathways enriched in the bronchial epithelium during asthma. We then explored a large number of datasets to identify possible confounders that may affect the POSTN gene expression and consequently, its interpretation as a reliable biomarker for asthma. Plasma and saliva levels of POSTN were determined in locally recruited asthmatic patients (mild, moderate and severe) compared to healthy controls to confirm the bioinformatics findings. Results: Our bioinformatics results confirmed that POSTN was consistently upregulated in the bronchial epithelium in asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) bronchial epithelium. In asthma, its mRNA expression was affected by gender, sample anatomical site and type, steroid therapy, and smoking. In our cohort, plasma POSTN was upregulated in severe and non-severe asthmatic patients. Saliva POSTN was significantly higher in non-severe asthmatic patients compared to healthy and severe asthmatic patients (specifically those who are not on Xolair (omalizumab)). Patients’ BMI, inhaled steroid use and Xolair treatment affected POSTN plasma levels. Conclusion: Up to our knowledge, this is the first study examining the level of POSTN in the saliva of asthmatic patients. Both plasma and saliva POSTN levels can aid in early diagnosis of asthma. Saliva POSTN level was more sensitive than plasma POSTN in differentiating between severe and non-severe asthmatics. Patients’ characteristics like BMI, the use of inhaled steroids, or Xolair treatment should be carefully reviewed before any meaningful interpretation of POSTN level in clinical practice.

ACS Style

Mahmood Yaseen Hachim; Noha Mousaad Elemam; Rakhee K Ramakrishnan; Ibrahim Yaseen Hachim; Laila Salameh; Bassam Mahboub; Saba Al Heialy; Rabih Halwani; Rifat Hamoudi; Qutayba Hamid. Confounding Patient Factors Affecting the Proper Interpretation of the Periostin Level as a Biomarker in Asthma Development. Journal of Asthma and Allergy 2020, ume 13, 23 -37.

AMA Style

Mahmood Yaseen Hachim, Noha Mousaad Elemam, Rakhee K Ramakrishnan, Ibrahim Yaseen Hachim, Laila Salameh, Bassam Mahboub, Saba Al Heialy, Rabih Halwani, Rifat Hamoudi, Qutayba Hamid. Confounding Patient Factors Affecting the Proper Interpretation of the Periostin Level as a Biomarker in Asthma Development. Journal of Asthma and Allergy. 2020; ume 13 ():23-37.

Chicago/Turabian Style

Mahmood Yaseen Hachim; Noha Mousaad Elemam; Rakhee K Ramakrishnan; Ibrahim Yaseen Hachim; Laila Salameh; Bassam Mahboub; Saba Al Heialy; Rabih Halwani; Rifat Hamoudi; Qutayba Hamid. 2020. "Confounding Patient Factors Affecting the Proper Interpretation of the Periostin Level as a Biomarker in Asthma Development." Journal of Asthma and Allergy ume 13, no. : 23-37.

Original research article
Published: 06 November 2019 in Frontiers in Endocrinology
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Previous work has shown that reduced expression of PLCXD3, a member of the phosphoinositide-specific phospholipases (PI-PLC) family, impaired insulin secretion with an unclear mechanism. In the current study, we aim to investigate the mechanism underlying this effect using human islets and rat INS-1 (832/13) cells. Microarray and RNA sequencing data showed that PLCXD3 is among the highly expressed PI-PLCs in human islets and INS-1 (832/13) cells. Expression of PLCXD3 was reduced in human diabetic islets, correlated positively with Insulin and GLP1R expression and inversely with the donor's body mass index (BMI) and glycated hemoglobin (HbA1c). Expression silencing of PLCXD3 in INS-1 (832/13) cells was found to reduce glucose-stimulated insulin secretion (GSIS) and insulin content. In addition, the expression of Insulin, NEUROD1, GLUT2, GCK, INSR, IRS2, and AKT was downregulated. Cell viability and apoptosis rate were unaffected. In conclusion, our data suggest that low expression of PLCXD3 in pancreatic β-cells associates with downregulation of the key insulin signaling and insulin biosynthesis genes as well as reduction in glucose sensing.

ACS Style

Hayat Aljaibeji; Debasmita Mukhopadhyay; Abdul Khader Mohammed; Sarah Dhaiban; Mahmood Hachim; Noha Mousaad Elemam; Nabil Sulaiman; Albert Salehi; Jalal Taneera. Reduced Expression of PLCXD3 Associates With Disruption of Glucose Sensing and Insulin Signaling in Pancreatic β-Cells. Frontiers in Endocrinology 2019, 10, 735 .

AMA Style

Hayat Aljaibeji, Debasmita Mukhopadhyay, Abdul Khader Mohammed, Sarah Dhaiban, Mahmood Hachim, Noha Mousaad Elemam, Nabil Sulaiman, Albert Salehi, Jalal Taneera. Reduced Expression of PLCXD3 Associates With Disruption of Glucose Sensing and Insulin Signaling in Pancreatic β-Cells. Frontiers in Endocrinology. 2019; 10 ():735.

Chicago/Turabian Style

Hayat Aljaibeji; Debasmita Mukhopadhyay; Abdul Khader Mohammed; Sarah Dhaiban; Mahmood Hachim; Noha Mousaad Elemam; Nabil Sulaiman; Albert Salehi; Jalal Taneera. 2019. "Reduced Expression of PLCXD3 Associates With Disruption of Glucose Sensing and Insulin Signaling in Pancreatic β-Cells." Frontiers in Endocrinology 10, no. : 735.

Original research
Published: 01 October 2019 in ImmunoTargets and Therapy
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Introduction: Although natural killer (NK) are major cells used to treat cancer patients, recent clinical trials showed that NK92 cells can be also used for the same purpose due to their high anti-tumor activity. Here, we examined whether these cells might be inflammatory due to the release of interleukin-1β (IL-1β), and whether the anti-inflammatory molecules dimethyl fumarate (DMF), or monomethyl fumarate (MMF) impair this activity. Methods: NK92 cells were examined for the synthesis and release of IL-1β utilizing RT-PCR and ELISA assay, respectively. The expression of hydroxy-carboxylic acid receptors (HCA)1, HCA2 and HCA3 was detected by immunoblotting, flow cytometry, immunofluorescence and RT-PCR assays. The activation of caspase-1 and Gasdermin D (GSDMD) was evaluated by immunoblot assay. Pyroptosis was demonstrated by immunofluorescence imaging. Expression of DNA methyltransferases (DNMTs) mRNA was determined by whole transcriptome and immunoblot analyses. Results: LPS-induced the release of IL-1β from NK92 cells, whereas DMF or MMF inhibited this induction. The effect of these drugs was due to inhibiting the conversion of procaspase-1 into active caspase-1. NK92 cells highly expressed GSDMD, a pyroptotic-mediated molecule. However, LPS induced the distribution of GSDMD into the cell membranes, corroborated with the presence of pyroptotic bodies, an activity that was inhibited by DMF or MMF. These molecule also inhibited the generation of GSDMD through DNMT-mediated hypermethylation of the promoter region of GSDMD gene. These results were supported by increased expression of DNMTs mRNA as determined by whole transcriptome analysis. Discussion: Our results are the first to show that NK92 cells utilize GSDMD pathway to release IL-1β. Further, DMF and MMF which were previously shown to enhance NK cell cytotoxicity, also inhibit the inflammatory effects of these cells, making them most suitable for treating cancer patients.

ACS Style

Jibran Sualeh Muhammad; Manju Nidagodu Jayakumar; Noha Mousaad Elemam; Thenmozhi Venkatachalam; Tom Kalathil Raju; Rifat Akram Hamoudi; Azzam A. Maghazachi. Gasdermin D Hypermethylation Inhibits Pyroptosis And LPS-Induced IL-1β Release From NK92 Cells. ImmunoTargets and Therapy 2019, ume 8, 29 -41.

AMA Style

Jibran Sualeh Muhammad, Manju Nidagodu Jayakumar, Noha Mousaad Elemam, Thenmozhi Venkatachalam, Tom Kalathil Raju, Rifat Akram Hamoudi, Azzam A. Maghazachi. Gasdermin D Hypermethylation Inhibits Pyroptosis And LPS-Induced IL-1β Release From NK92 Cells. ImmunoTargets and Therapy. 2019; ume 8 ():29-41.

Chicago/Turabian Style

Jibran Sualeh Muhammad; Manju Nidagodu Jayakumar; Noha Mousaad Elemam; Thenmozhi Venkatachalam; Tom Kalathil Raju; Rifat Akram Hamoudi; Azzam A. Maghazachi. 2019. "Gasdermin D Hypermethylation Inhibits Pyroptosis And LPS-Induced IL-1β Release From NK92 Cells." ImmunoTargets and Therapy ume 8, no. : 29-41.

Journal article
Published: 21 September 2019 in Molecular and Cellular Endocrinology
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The expression and functional impact of most orphan G-protein coupled receptors (GPCRs) in β-cell is not fully understood. Microarray expression indicated that 36 orphan GPCRs are restricted in human islets, while 55 receptors overlapped between human islets and INS-1 cells. GPR183 showed higher expression in diabetic compared to non-diabetic human islets. GPR183 expression co-localized with β-cells while it was lacking in α-cells in human islets. The GPR183 agonist (7α-25-DHC) potentiated insulin secretion and protected against glucotoxicity-induced β-cell damage in human islets. Silencing of GPR183 in INS-1 cells decreased the expression of proinsulin genes, Pdx1, Mafa and impaired insulin secretion with a concomitant decrease in cAMP generation. Cultured INS-1 cells with 7α-25-DHC were associated with increased proliferation and expression of GPR183, INS2, PDX1, NeuroD, and INSR. In conclusion, the beneficial impact of GPR183 activation on β-cell function makes it a potential therapeutic target to prevent or reverse β-cell dysfunction.

ACS Style

Jalal Taneera; Israa Mohammed; Abdul Khader Mohammed; Mahmood Hachim; Sarah Dhaiban; Abdullah Malek; Pontus Dunér; Noha M. Elemam; Nabil Sulaiman; Mawieh Hamad; Albert Salehi. Orphan G-protein coupled receptor 183 (GPR183) potentiates insulin secretion and prevents glucotoxicity-induced β-cell dysfunction. Molecular and Cellular Endocrinology 2019, 499, 110592 .

AMA Style

Jalal Taneera, Israa Mohammed, Abdul Khader Mohammed, Mahmood Hachim, Sarah Dhaiban, Abdullah Malek, Pontus Dunér, Noha M. Elemam, Nabil Sulaiman, Mawieh Hamad, Albert Salehi. Orphan G-protein coupled receptor 183 (GPR183) potentiates insulin secretion and prevents glucotoxicity-induced β-cell dysfunction. Molecular and Cellular Endocrinology. 2019; 499 ():110592.

Chicago/Turabian Style

Jalal Taneera; Israa Mohammed; Abdul Khader Mohammed; Mahmood Hachim; Sarah Dhaiban; Abdullah Malek; Pontus Dunér; Noha M. Elemam; Nabil Sulaiman; Mawieh Hamad; Albert Salehi. 2019. "Orphan G-protein coupled receptor 183 (GPR183) potentiates insulin secretion and prevents glucotoxicity-induced β-cell dysfunction." Molecular and Cellular Endocrinology 499, no. : 110592.

Original research
Published: 01 August 2019 in Pharmacogenomics and Personalized Medicine
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Background: With the increasing incidence of asthma, more attention is focused on the diverse and complex nutritional and environmental triggers of asthma exacerbations. Currently, there are no established risk assessment tools to evaluate asthma triggering potentials of most of the nutritional and environmental triggers encountered by asthmatic patients. Purpose: The objective of this study is to devise a reliable workflow, capable of estimating the toxicogenomic effect of such factors on key player genes in asthma pathogenesis. Methods: Gene expression extracted from publicly available datasets of asthmatic bronchial epithelium were subjected to a comprehensive analysis of differential gene expression to identify significant genes involved in asthma development and progression. The identified genes were subjected to Gene Set Enrichment Analysis using a total of 31,826 gene sets related to chemical, toxins, and drugs to identify common agents that share similar asthma-related targets genes and signaling pathways. Results: Our analysis identified 225 differentially expressed genes between severe asthmatic and healthy bronchial epithelium. Gene Set Enrichment Analysis of the identified genes showed that they are involved in response to toxic substances and organic cyclic compounds and are targeted by 41 specific diets, plants products, and plants related toxins (eg adenine, arachidonic acid, baicalein, caffeic acid, corilagin, curcumin, ellagic acid, luteolin, microcystin-RR, phytoestrogens, protoporphyrin IX, purpurogallin, rottlerin, and salazinic acid). Moreover, the identified chemicals share interesting inflammation-related pathways like NF-κB. Conclusion: Our analysis was able to explain and predict the toxicity in terms of stimulating the differentially expressed genes between severe asthmatic and healthy epithelium. Such an approach can pave the way to generate a cost-effective and reliable source for asthma-specific toxigenic reports thus allowing the asthmatic patients, physicians, and medical researchers to be aware of the potential triggering factors with fatal consequences.

ACS Style

Mahmood Yaseen Hachim; Ibrahim Yaseen Hachim; Noha M. Elemam; Rifat A Hamoudi. Toxicogenomic analysis of publicly available transcriptomic data can predict food, drugs, and chemical-induced asthma. Pharmacogenomics and Personalized Medicine 2019, ume 12, 181 -199.

AMA Style

Mahmood Yaseen Hachim, Ibrahim Yaseen Hachim, Noha M. Elemam, Rifat A Hamoudi. Toxicogenomic analysis of publicly available transcriptomic data can predict food, drugs, and chemical-induced asthma. Pharmacogenomics and Personalized Medicine. 2019; ume 12 ():181-199.

Chicago/Turabian Style

Mahmood Yaseen Hachim; Ibrahim Yaseen Hachim; Noha M. Elemam; Rifat A Hamoudi. 2019. "Toxicogenomic analysis of publicly available transcriptomic data can predict food, drugs, and chemical-induced asthma." Pharmacogenomics and Personalized Medicine ume 12, no. : 181-199.

Original article
Published: 04 April 2019 in Archives of Virology
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Epigallocatechin gallate (EGCG) is the most abundant component in green tea extract, that has powerful antioxidant and antiviral effects. It has been previously reported to inhibit HCV entry via several mechanisms. Hence, this study aimed at further investigating the potential impact of EGCG on HCV entry through regulation of the expression of tetraspanin receptor CD81 by the novel predicted miR-548m. Liver biopsies were obtained from 29 HCV patients and 10 healthy controls for expression profiling. Huh7 cells were stimulated with EGCG and subsequently miR-548m expression was assessed. Naïve, HCV- ED43/JFH-1 and HCV-JFH-1 infected Huh7 cells were transfected by miR-548m mimics and inhibitors. Consequently, CD81 protein and mRNA levels were assessed using flow cytometry and qRT-PCR, respectively. Additionally, these cells were used to investigate HCV permissiveness into Huh7 cells using qRT-PCR for viral quantification. Direct binding confirmation of miR-548m to CD81 was done using luciferase reporter assay. In-silico analysis revealed miR-548m to have two potential binding sites in the 3’UTR of CD81 mRNA. EGCG boosted miR-548m expression in Huh7 cells. Additionally, miR-548m caused a downregulation of CD81 protein and mRNA levels as well as reduction in HCV infectivity of Huh7 cells. Luciferase binding assay confirmed the binding of miR-548m to CD81 mRNA at the two predicted binding sites. Intriguingly, miR-548m expression was not detected in healthy liver biopsies but was found in liver biopsies of HCV patients. This study shows that EGCG might act as an anti-HCV agent that reduces cellular infectivity via enhancing miR-548m expression and repressing CD81 receptor.

ACS Style

Radwa Yehia Mekky; Nada El-Ekiaby; Shereen Ahmed El Sobky; Noha Mousaad Elemam; Rana Ahmed Youness; Mohammad El-Sayed; Mohammed Tarif Hamza; Gamal Esmat; Ahmed Ihab Abdelaziz. Epigallocatechin gallate (EGCG) and miR-548m reduce HCV entry through repression of CD81 receptor in HCV cell models. Archives of Virology 2019, 164, 1587 -1595.

AMA Style

Radwa Yehia Mekky, Nada El-Ekiaby, Shereen Ahmed El Sobky, Noha Mousaad Elemam, Rana Ahmed Youness, Mohammad El-Sayed, Mohammed Tarif Hamza, Gamal Esmat, Ahmed Ihab Abdelaziz. Epigallocatechin gallate (EGCG) and miR-548m reduce HCV entry through repression of CD81 receptor in HCV cell models. Archives of Virology. 2019; 164 (6):1587-1595.

Chicago/Turabian Style

Radwa Yehia Mekky; Nada El-Ekiaby; Shereen Ahmed El Sobky; Noha Mousaad Elemam; Rana Ahmed Youness; Mohammad El-Sayed; Mohammed Tarif Hamza; Gamal Esmat; Ahmed Ihab Abdelaziz. 2019. "Epigallocatechin gallate (EGCG) and miR-548m reduce HCV entry through repression of CD81 receptor in HCV cell models." Archives of Virology 164, no. 6: 1587-1595.