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Cyrille Mathieu; Marion Ferren; Olivia Harder; Francesca T. Bovier; Tara C. Marcink; Camilla Predella; Fabrizio Angius; Jennifer Drew-Bear; N. Valerio Dorrello; Alex L. Greninger; Anne Moscona; Stefan Niewiesk; Branka Horvat; Matteo Porotto. Single-chain variable fragment antibody constructs neutralize measles virus infection in vitro and in vivo. Cellular & Molecular Immunology 2021, 1 -3.
AMA StyleCyrille Mathieu, Marion Ferren, Olivia Harder, Francesca T. Bovier, Tara C. Marcink, Camilla Predella, Fabrizio Angius, Jennifer Drew-Bear, N. Valerio Dorrello, Alex L. Greninger, Anne Moscona, Stefan Niewiesk, Branka Horvat, Matteo Porotto. Single-chain variable fragment antibody constructs neutralize measles virus infection in vitro and in vivo. Cellular & Molecular Immunology. 2021; ():1-3.
Chicago/Turabian StyleCyrille Mathieu; Marion Ferren; Olivia Harder; Francesca T. Bovier; Tara C. Marcink; Camilla Predella; Fabrizio Angius; Jennifer Drew-Bear; N. Valerio Dorrello; Alex L. Greninger; Anne Moscona; Stefan Niewiesk; Branka Horvat; Matteo Porotto. 2021. "Single-chain variable fragment antibody constructs neutralize measles virus infection in vitro and in vivo." Cellular & Molecular Immunology , no. : 1-3.
Oncogenic and latent-persistent viruses belonging to both DNA and RNA groups are known to cause serious metabolism alterations. Among these, the Human Herpesvirus 8 (HHV8) infection induces stable modifications in biochemistry and cellular metabolism, which in turn affect its own pathological properties. HHV8 enhances the expression of insulin receptors, supports the accumulation of neutral lipids in cytoplasmic lipid droplets and induces alterations in both triglycerides and cholesterol metabolism in endothelial cells. In addition, HHV8 is also known to modify immune response and cytokine production with implications for cell oxidative status (i.e., reactive oxygen species activation). This review underlines the recent findings regarding the role of latent and persistent HHV8 viral infection in host physiology and pathogenesis.
Fabrizio Angius; Angela Ingianni; Raffaello Pompei. Human Herpesvirus 8 and Host-Cell Interaction: Long-Lasting Physiological Modifications, Inflammation and Related Chronic Diseases. Microorganisms 2020, 8, 388 .
AMA StyleFabrizio Angius, Angela Ingianni, Raffaello Pompei. Human Herpesvirus 8 and Host-Cell Interaction: Long-Lasting Physiological Modifications, Inflammation and Related Chronic Diseases. Microorganisms. 2020; 8 (3):388.
Chicago/Turabian StyleFabrizio Angius; Angela Ingianni; Raffaello Pompei. 2020. "Human Herpesvirus 8 and Host-Cell Interaction: Long-Lasting Physiological Modifications, Inflammation and Related Chronic Diseases." Microorganisms 8, no. 3: 388.
Objective To investigate the link between Human Herpesvirus 8 (HHV8) infection and plasma oxidative stress in patients with diabetes mellitus type 2 (DM2). Results Blood samples collected from DM2 and control subjects were screened for the presence of antibodies against HHV8 and for biomarkers of oxidative stress. We determined the products of radical damage on the plasma lipid fraction, such as malondialdehyde (MDA), fatty acid hydroperoxides (HP) and 7-ketocholesterol (7-keto), the oxidation products of unsaturated fatty acids (UFA) and cholesterol, respectively. The level of plasma antioxidant α-tocopherol (α-toc) was also assessed. Relevant differences were observed in the redox status in DM2 and either HHV8-positive or -negative control subjects. The level of α-toc significantly decreased in both DM2 and HHV8-positive subjects. Levels of MDA, HP and 7-keto were much higher in HHV8-positive and DM2 subjects, indicating that plasma oxidative stress is a common feature in both DM2 and HHV8-infection. In addition, 7-keto was further increased in HHV8-positive DM2 patients. We hypothesized that the HHV8-infection may contribute to the production of ROS, and hence to the oxidative stress closely related to the pathogenesis and development of DM2.
Alessandra Incani; Luisa Marras; Gabriele Serreli; Angela Ingianni; Raffaello Pompei; Monica Deiana; Fabrizio Angius. Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients. BMC Research Notes 2020, 13, 1 -6.
AMA StyleAlessandra Incani, Luisa Marras, Gabriele Serreli, Angela Ingianni, Raffaello Pompei, Monica Deiana, Fabrizio Angius. Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients. BMC Research Notes. 2020; 13 (1):1-6.
Chicago/Turabian StyleAlessandra Incani; Luisa Marras; Gabriele Serreli; Angela Ingianni; Raffaello Pompei; Monica Deiana; Fabrizio Angius. 2020. "Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients." BMC Research Notes 13, no. 1: 1-6.
Introduction: Human Herpesvirus 8 (HHV8) is known to be the cause of the malignant tumour named Kaposi’s sarcoma. It is believed to induce an intense modification of cell metabolism in endothelial cells. In this work we analysed the role of anti-HHV8 antibodies in both the insulin and glucose uptake of HHV8-infected primary human endothelial cells (HUVEC). Methodology: Western blotting, immunofluorescence and radiolabelled glucose were employed to assess the pPI3K expression, insulin binding and glucose-uptake by HUVEC cells, respectively. Results: We confirmed that HHV8-infection is able to enhance both insulin binding and glucose-uptake in HHV8-infected primary endothelial cells; in addition, we found that anti-HHV8 specific antibodies are able to further increase both insulin and glucose uptake during the late latent phase of HHV8-infection in vitro. Conclusions: These findings suggest that a specific immune response to HHV8-infection may cooperate in boosting the cell metabolism, further enhancing the already increased insulin binding and glucose-uptake in HHV8-infected cells, which is a peculiar property of several oncogenic viruses.
Fabrizio Angius; Enrica Piras; Stefano Spolitu; Luisa Marras; Sara Federica Armas; Angela Ingianni; Pierpaolo Contini; Raffaello Pompei. Anti-Human Herpesvirus 8 antibodies affect both insulin and glucose uptake by virus-infected human endothelial cells. The Journal of Infection in Developing Countries 2018, 12, 485 -491.
AMA StyleFabrizio Angius, Enrica Piras, Stefano Spolitu, Luisa Marras, Sara Federica Armas, Angela Ingianni, Pierpaolo Contini, Raffaello Pompei. Anti-Human Herpesvirus 8 antibodies affect both insulin and glucose uptake by virus-infected human endothelial cells. The Journal of Infection in Developing Countries. 2018; 12 (6):485-491.
Chicago/Turabian StyleFabrizio Angius; Enrica Piras; Stefano Spolitu; Luisa Marras; Sara Federica Armas; Angela Ingianni; Pierpaolo Contini; Raffaello Pompei. 2018. "Anti-Human Herpesvirus 8 antibodies affect both insulin and glucose uptake by virus-infected human endothelial cells." The Journal of Infection in Developing Countries 12, no. 6: 485-491.
Background and Purpose Microglia phenotype and phagocytic activity are deregulated in Parkinson's disease (PD). Peroxisome proliferator‐activated receptor gamma (PPARγ) agonists are neuroprotective in experimental PD, but their role in regulating microglial phenotype and phagocytosis has been poorly investigated. We addressed it by using the PPARγ agonist MDG548. Experimental Approach Murine microglial cell line MMGT12 was stimulated with LPS and/or MDG548 and their effect on phagocytosis of fluorescent microspheres or necrotic neurons was investigated by flow cytometry. Cytokines and markers of microglia phenotype such as Mannose Receptor C‐Type 1 (MRC1), Ym1 and CD68 were measured by ELISA and fluorescent immunohistochemistry. Levels of Beclin‐1, recently shown to play a role in microglial phagocytosis, were measured by western blotting. In the In vivo MPTP‐probenecid (MPTPp) model of PD in mice, MDG548 was tested on motor impairment, nigral neurodegeneration, microglial activation and phenotype. Key Results MDG548, applied to LPS‐stimulated microglia, increased the phagocytosis of both latex beads and necrotic cells, upregulated the expression of MRC1, CD68 and to a lesser extent IL‐10, while counteracted the LPS‐induced increase of TNF‐α and iNOS. MDG548 also caused the induction of Beclin‐1. The chronic MPTPp treatment in mice downregulated MRC1 and TGF‐β and upregulated TNF‐α and IL‐1β immunoreactivity in activated CD11b‐positive microglia, causing the death of nigral dopaminergic neurons. MDG548 arrested the MPTPp‐induced cell death, enhanced MRC1 and restored cytokines levels. Conclusion and Implications This study adds a novel mechanism for PPARγ‐mediated neuroprotection in PD, and suggests that boosting the phagocytic activity and anti‐inflammatory markers may represent an effective disease‐modifying approach.
Daniela Lecca; Elzbieta Janda; Giovanna Mulas; Andrea Diana; Concetta Martino; Fabrizio Angius; Stefano Spolitu; Maria Antonietta Casu; Gabriella Simbula; Laura Boi; Barbara Batetta; Saturnino Spiga; Anna R Carta. Boosting phagocytosis and anti-inflammatory phenotype in microglia mediates neuroprotection by PPARγ agonist MDG548 in Parkinson's disease models. Journal of Cerebral Blood Flow & Metabolism 2018, 175, 3298 -3314.
AMA StyleDaniela Lecca, Elzbieta Janda, Giovanna Mulas, Andrea Diana, Concetta Martino, Fabrizio Angius, Stefano Spolitu, Maria Antonietta Casu, Gabriella Simbula, Laura Boi, Barbara Batetta, Saturnino Spiga, Anna R Carta. Boosting phagocytosis and anti-inflammatory phenotype in microglia mediates neuroprotection by PPARγ agonist MDG548 in Parkinson's disease models. Journal of Cerebral Blood Flow & Metabolism. 2018; 175 (16):3298-3314.
Chicago/Turabian StyleDaniela Lecca; Elzbieta Janda; Giovanna Mulas; Andrea Diana; Concetta Martino; Fabrizio Angius; Stefano Spolitu; Maria Antonietta Casu; Gabriella Simbula; Laura Boi; Barbara Batetta; Saturnino Spiga; Anna R Carta. 2018. "Boosting phagocytosis and anti-inflammatory phenotype in microglia mediates neuroprotection by PPARγ agonist MDG548 in Parkinson's disease models." Journal of Cerebral Blood Flow & Metabolism 175, no. 16: 3298-3314.
Commentary: High Glucose Induces Reactivation of Latent Kaposi's Sarcoma-Associated Herpesvirus
Fabrizio Angius; Maria A. Madeddu; Raffaello Pompei. Commentary: High Glucose Induces Reactivation of Latent Kaposi's Sarcoma-Associated Herpesvirus. Frontiers in Microbiology 2017, 8, 1796 .
AMA StyleFabrizio Angius, Maria A. Madeddu, Raffaello Pompei. Commentary: High Glucose Induces Reactivation of Latent Kaposi's Sarcoma-Associated Herpesvirus. Frontiers in Microbiology. 2017; 8 ():1796.
Chicago/Turabian StyleFabrizio Angius; Maria A. Madeddu; Raffaello Pompei. 2017. "Commentary: High Glucose Induces Reactivation of Latent Kaposi's Sarcoma-Associated Herpesvirus." Frontiers in Microbiology 8, no. : 1796.
Kaposi sarcoma herpesvirus (KSHV), also known as human herpesvirus 8, is the causative agent of Kaposi sarcoma; this malignant angiosarcoma is usually treated with conventional antitumor agents that can control disease evolution, but do not clear the latent KSHV episome that binds to cellular DNA. Some commercial antibacterial sulfonamides were tested for the ability to suppress latent KSHV. Quantitative PCR (qPCR) and cytofluorometry assays were used for detecting both viral DNA and the latency factor LANA (latency-associated nuclear antigen) in BC3 cells, respectively. The capacity of sulfonamides to impair MDM2-p53 complex formation was detected by an enzyme-linked immunosorbent assay method. The analysis of variance was performed according to one-way analysis of variance with Fisher as a post hoc test. Here we show that sulfonamide antibiotics are able to suppress the KSHV latent state in permanently infected BC3 lymphoma cells and interfere with the formation of the MDM2-p53 complex that KSHV seemingly needs to support latency and to trigger tumor cell transformation. These findings detected a new molecular target for the activity of sulfonamides and offer a new potential perspective for treating KSHV-induced lymphoproliferative diseases.
Fabrizio Angius; Enrica Piras; Sabrina Uda; Clelia Madeddu; Roberto Serpe; Rachele Bigi; Wuguo Chen; Dirk Dittmer; Raffaello Pompei; Angela Ingianni. Antimicrobial sulfonamides clear latent Kaposi sarcoma herpesvirus infection and impair MDM2-p53 complex formation. The Journal of Antibiotics 2017, 70, 962 -966.
AMA StyleFabrizio Angius, Enrica Piras, Sabrina Uda, Clelia Madeddu, Roberto Serpe, Rachele Bigi, Wuguo Chen, Dirk Dittmer, Raffaello Pompei, Angela Ingianni. Antimicrobial sulfonamides clear latent Kaposi sarcoma herpesvirus infection and impair MDM2-p53 complex formation. The Journal of Antibiotics. 2017; 70 (9):962-966.
Chicago/Turabian StyleFabrizio Angius; Enrica Piras; Sabrina Uda; Clelia Madeddu; Roberto Serpe; Rachele Bigi; Wuguo Chen; Dirk Dittmer; Raffaello Pompei; Angela Ingianni. 2017. "Antimicrobial sulfonamides clear latent Kaposi sarcoma herpesvirus infection and impair MDM2-p53 complex formation." The Journal of Antibiotics 70, no. 9: 962-966.
In the present work, silver nanoparticles were prepared using a totally green procedure combining silver nitrate and an extract of grape pomace as a green source. Additionally, nanoparticles were stabilized using phospholipid and water and/or a mixture of water and propylene glycol (PG). To the best of our knowledge, grape-silver nanoparticle stabilized liposomes or PG-liposomes were formulated, for the first time, combining the residual products of wine-made industry, silver nitrate and phospholipids, avoiding the addition of hazardous substances to human health and the environment, in an easy, scalable and reproducible method. The structure and morphology of grape-silver nanoparticle stabilized vesicles were evaluated by transmission electron microscopy (TEM), UV-vis spectroscopy and photon correlation spectroscopy. Samples were designed as possible carrier for skin protection because of their double function: the grape extract acts as antioxidant and the colloidal silver as antimicrobial agent, which might be helpful in eliminating dangerous free radicals and many pathogenic microorganisms. Obtained nanoparticles were small in size and their combination with phospholipids did not hamper the vesicle formation, which were multilamellar and sized ~100nm. TEM images shows a heterogeneous distribution of nanoparticles, which were located both in the intervesicular medium and in the vesicular structure. Further, grape-silver nanoparticles, when stabilized by liposomes, were able to inhibit the proliferation of both Staphylococcus aureus and Pseudomonas aeruginosa and provided a great protection of keratinocytes and fibroblasts against oxidative stress avoiding their damage and death.
Ines Castangia; Francesca Marongiu; Maria Letizia Manca; Raffaello Pompei; Fabrizio Angius; Andrea Ardu; Anna Maria Fadda; Maria Manconi; Guido Ennas. Combination of grape extract-silver nanoparticles and liposomes: A totally green approach. European Journal of Pharmaceutical Sciences 2017, 97, 62 -69.
AMA StyleInes Castangia, Francesca Marongiu, Maria Letizia Manca, Raffaello Pompei, Fabrizio Angius, Andrea Ardu, Anna Maria Fadda, Maria Manconi, Guido Ennas. Combination of grape extract-silver nanoparticles and liposomes: A totally green approach. European Journal of Pharmaceutical Sciences. 2017; 97 ():62-69.
Chicago/Turabian StyleInes Castangia; Francesca Marongiu; Maria Letizia Manca; Raffaello Pompei; Fabrizio Angius; Andrea Ardu; Anna Maria Fadda; Maria Manconi; Guido Ennas. 2017. "Combination of grape extract-silver nanoparticles and liposomes: A totally green approach." European Journal of Pharmaceutical Sciences 97, no. : 62-69.
Neuroinflammation is associated with l-DOPA treatment in Parkinson's disease (PD), suggesting a role in l-DOPA-induced dyskinesia (LID), however it is unclear whether increased inflammation is specifically related to the dyskinetic outcome of l-DOPA treatment. Diversely from oral l-DOPA, continuous intrajejunal l-DOPA infusion is associated with very low dyskinetic outcome in PD patients. We reproduced these regimens of administration in 6-OHDA-lesioned hemiparkinsonian rats, where dyskinetic responses and striatal neuroinflammation induced by chronic pulsatile (DOPAp) or continuous (DOPAc) l-DOPA were compared. Moreover, we investigated the contribution of a peripheral inflammatory challenge with lipopolysaccharide (LPS), to DOPAp-induced dyskinetic and neuroinflammatory responses. Rats 6-OHDA-infused in the medial forebrain bundle received two weeks treatment with DOPAp, DOPAc via subcutaneous osmotic minipumps, or DOPAp followed by DOPAc. l-DOPA plasma levels were measured in all experimental groups. An independent group of rats received one peripheral dose of LPS 24h before DOPAp treatment. Abnormal involuntary movements (AIMs) were evaluated as a rat model of LID. Immunoreactivity (IR) for OX-42, microglial and neuronal TNF-α, iNOS and GFAP was quantified in denervated and contralateral striatum. In addition, serum TNF-α was measured. The 6-OHDA denervation induced a mild microgliosis in the striatum two weeks after neurotoxin infusion, and increased TNF-α IR in microglia. Rats receiving the DOPAp treatment developed AIMs and displayed increased striatal OX-42, microglial TNF-α, iNOS and GFAP. Moreover, TNF-α IR was also increased in a subpopulation of striatal neurons. Conversely, DOPAc did not induce AIMs or inflammatory responses in either drug-naïve animals or rats that were previously dyskinetic when exposed to DOPAp. Serum TNF-α was not altered by any l-DOPA treatment. LPS pre-treatment increased the degree of DOPAp-induced AIMs and striatal IR for OX-42, TNF-α, iNOS and GFAP. Altogether the present findings indicate that in the 6-OHDA model, chronic l-DOPA induces striatal inflammatory responses, which however depend upon the administration regimen and the dyskinetic outcome of drug treatment. The potentiation of dyskinetic responses by LPS suggests a reciprocal causal link between neuroinflammation and LID.
Giovanna Mulas; Elena Espa; Sandro Fenu; Saturnino Spiga; Giovanni Cossu; Elisabetta Pillai; Ezio Carboni; Gabriella Simbula; Dragana Jadžić; Fabrizio Angius; Stefano Spolitu; Barbara Batetta; Daniela Lecca; Andrea Giuffrida; Anna R. Carta. Differential induction of dyskinesia and neuroinflammation by pulsatile versus continuous l -DOPA delivery in the 6-OHDA model of Parkinson's disease. Experimental Neurology 2016, 286, 83 -92.
AMA StyleGiovanna Mulas, Elena Espa, Sandro Fenu, Saturnino Spiga, Giovanni Cossu, Elisabetta Pillai, Ezio Carboni, Gabriella Simbula, Dragana Jadžić, Fabrizio Angius, Stefano Spolitu, Barbara Batetta, Daniela Lecca, Andrea Giuffrida, Anna R. Carta. Differential induction of dyskinesia and neuroinflammation by pulsatile versus continuous l -DOPA delivery in the 6-OHDA model of Parkinson's disease. Experimental Neurology. 2016; 286 ():83-92.
Chicago/Turabian StyleGiovanna Mulas; Elena Espa; Sandro Fenu; Saturnino Spiga; Giovanni Cossu; Elisabetta Pillai; Ezio Carboni; Gabriella Simbula; Dragana Jadžić; Fabrizio Angius; Stefano Spolitu; Barbara Batetta; Daniela Lecca; Andrea Giuffrida; Anna R. Carta. 2016. "Differential induction of dyskinesia and neuroinflammation by pulsatile versus continuous l -DOPA delivery in the 6-OHDA model of Parkinson's disease." Experimental Neurology 286, no. : 83-92.
The prevalence of Human Herpesvirus 8 (HHV8) DNA and antiviral antibodies in Diabetes type 2 (DM2) and control subjects was studied, in order to confirm a possible link between DM2 and HHV8 infection. The HHV8-DNA from diabetic patients was typed for detecting possible genomic differences with known HHV8 reference viruses.DM2 patients and healthy controls were examined for the presence of HHV8 DNA into the peripheral blood lymphocytes. Both anti-lytic and latent phase antibodies were detected in HHV8 positive and negative diabetic patients, as well in a number of controls. The HHV8 ORF K1 and ORF 26 genes from DM2 patients were typed and matched to reference strains.A significant prevalence of HHV8 DNA in DM2 subjects versus healthy controls was detected (about 58 % against 27 %). Anti-lytic phase, but not anti-latent phase antibodies, were significantly increased in DM2 patients versus controls. In addition, about 30 % of HHV8 strains isolated from DM2 lymphocytes showed consistent differences in the ORF 26 gene sequence, so that a new HHV8 subtype was proposed. These findings give additional support to the hypothesis that HHV8 could be considered an additional risk factor for DM2 onset.
Enrica Piras; Maria A. Madeddu; Giuseppina Palmieri; Fabrizio Angius; Pierpaolo Contini; Raffaello Pompei; Angela Ingianni. High Prevalence of Human Herpesvirus 8 Infection in Diabetes Type 2 Patients and Detection of a New Virus Subtype. Chemistry and Biology of Pteridines and Folates 2016, 973, 41 -51.
AMA StyleEnrica Piras, Maria A. Madeddu, Giuseppina Palmieri, Fabrizio Angius, Pierpaolo Contini, Raffaello Pompei, Angela Ingianni. High Prevalence of Human Herpesvirus 8 Infection in Diabetes Type 2 Patients and Detection of a New Virus Subtype. Chemistry and Biology of Pteridines and Folates. 2016; 973 ():41-51.
Chicago/Turabian StyleEnrica Piras; Maria A. Madeddu; Giuseppina Palmieri; Fabrizio Angius; Pierpaolo Contini; Raffaello Pompei; Angela Ingianni. 2016. "High Prevalence of Human Herpesvirus 8 Infection in Diabetes Type 2 Patients and Detection of a New Virus Subtype." Chemistry and Biology of Pteridines and Folates 973, no. : 41-51.
The fluorescence properties of colloidal sealed Rhodamine 6G doped mesostructured silica nanoparticles prepared by a one-pot templated base-catalyzed sol–gel self-assembly method are reported. The hybrid organic–inorganic nanoparticles is tested against water and alcohols dye leaching showing larger resilience to leaching in water, high quantum yield despite the large dye concentration and huge relative brightness up to 1.5 × 105 emitting molecules per nanoparticle. This super fluorescence is 3 times larger of comparable systems and 100 times larger than the fluorescence of CdSe/ZnS quantum dots. The surfactant used for the formation of the mesostructure plays a key role both as dye splitting element and as sealing agent against leaching effect. The resilience to dye leaching in water is further justified by the formation of core–shell architectures made up of mesoporous core and homogeneous low-porous silica shell of 5–12 nm in thickness due to long aging condensation reaction of surface silanols in water. In addition, the comparison with a reference no-doped silica sample points out a possible alternative synthetic strategy to tune the structural, morphological and textural properties of silica-based nanosystems: properly engineering can exploit the effect of dye molecules addition on nanoparticles mean size, polydispersity and mean thickness of matrix silica walls.
Carlo Maria Carbonaro; Federica Orrù; Pier Carlo Ricci; Andrea Ardu; Riccardo Corpino; Daniele Chiriu; Fabrizio Angius; Andrea Mura; Carla Cannas. High efficient fluorescent stable colloidal sealed dye-doped mesostructured silica nanoparticles. Microporous and Mesoporous Materials 2016, 225, 432 -439.
AMA StyleCarlo Maria Carbonaro, Federica Orrù, Pier Carlo Ricci, Andrea Ardu, Riccardo Corpino, Daniele Chiriu, Fabrizio Angius, Andrea Mura, Carla Cannas. High efficient fluorescent stable colloidal sealed dye-doped mesostructured silica nanoparticles. Microporous and Mesoporous Materials. 2016; 225 ():432-439.
Chicago/Turabian StyleCarlo Maria Carbonaro; Federica Orrù; Pier Carlo Ricci; Andrea Ardu; Riccardo Corpino; Daniele Chiriu; Fabrizio Angius; Andrea Mura; Carla Cannas. 2016. "High efficient fluorescent stable colloidal sealed dye-doped mesostructured silica nanoparticles." Microporous and Mesoporous Materials 225, no. : 432-439.
Tumor cells are characterised by a high content of cholesterol esters (CEs), while tumor-bearing patients show low levels of high-density lipoproteins (HDLs). The origin and significance of high CE levels in cancer cell biology has not been completely clarified. Recent evidence that lymphoblastic cells selectively acquire exogenous CE from HDL via the scavenger receptor SR-BI has drawn attention to the additional membrane proteins involved in this pathway. P-glycopotein-MDR1 (P-gp) is a product of the MDR1 gene and confers resistance to antitumor drugs. Its possible role in plasma membrane cholesterol trafficking and CE metabolism has been suggested. In the present study this aspect was investigated in a lymphoblastic cell line selected for MDR1 resistance. CEM were made resistant by stepwise exposure to low (LR) and high (HR) doses of vincristine (VCR). P-gp activity (3H-vinblastine), CE content, CE and triglycerides (TG) synthesis (14C-oleate), neutral lipids and Dil-HDL uptake (fluorescence), SR-BI, ABCA1 and P-gp protein expression (western blotting) were determined. To better evaluate the relationship between CE metabolism and P-gp activity, the ACAT inhibitor Sandoz-58035 and the P-gp inhibitors progesterone, cyclosporine and verapamil were used. CE content and synthesis were similar in the parental and resistant cells. However, in the latter population, SR-BI protein expression increased, whereas CE-HDL uptake decreased. These changes correlated with the degree of VCR-resistance. As well as reverting MDR1-resistance, the inhibitors of P-gp activity induced the CE-HDL/SR-BI pathway by reactivating membrane cholesterol trafficking. Indeed, CE-HDL uptake, SRBI expression and CE content increased, whereas there was a decrease in cholesterol esterification. These results demonstrated that P-gp overexpression impairs anticancer drug uptake as well as the SR-BI mediated selective CE-HDL uptake. This suggests that these membrane proteins act in an opposite manner on the same transport mechanism. Therefore, the dampening activity of P-gp in this pathway and its reversal by P-gp inhibitors open new strategies for antitumor therapy in drug-resistant tumors.
Stefano Spolitu; Sabrina Uda; Stefania Deligia; Alessandra Frau; Maria Collu; Fabrizio Angius; Barbara Batetta. Multidrug resistance P-glycoprotein dampens SR-BI cholesteryl ester uptake from high density lipoproteins in human leukemia cells. American journal of cancer research 2016, 6, 615 -627.
AMA StyleStefano Spolitu, Sabrina Uda, Stefania Deligia, Alessandra Frau, Maria Collu, Fabrizio Angius, Barbara Batetta. Multidrug resistance P-glycoprotein dampens SR-BI cholesteryl ester uptake from high density lipoproteins in human leukemia cells. American journal of cancer research. 2016; 6 (3):615-627.
Chicago/Turabian StyleStefano Spolitu; Sabrina Uda; Stefania Deligia; Alessandra Frau; Maria Collu; Fabrizio Angius; Barbara Batetta. 2016. "Multidrug resistance P-glycoprotein dampens SR-BI cholesteryl ester uptake from high density lipoproteins in human leukemia cells." American journal of cancer research 6, no. 3: 615-627.
High density lipoproteins (HDLs) play a crucial role in removing excess cholesterol from peripheral tissues. Although their concentration is lower during conditions of high cell growth rate (cancer and infections), their involvement during cell proliferation is not known. To this aim, we investigated the replicative cycles in synchronised Swiss 3T3 fibroblasts in different experimental conditions: i) contact-inhibited fibroblasts re-entering cell cycle after dilution; ii) scratch-wound assay; iii) serum-deprived cells induced to re-enter G1 by FCS, HDL or PDGF. Analyses were performed during each cell cycle up to quiescence. Cholesterol synthesis increased remarkably during the replicative cycles, decreasing only after cells reached confluence. In contrast, cholesteryl ester (CE) synthesis and content were high at 24 h after dilution and then decreased steeply in the successive cycles. Flow cytometry analysis of DiO-HDL, as well as radiolabeled HDL pulse, demonstrated a significant uptake of CE-HDL in 24 h. DiI-HDL uptake, lipid droplets (LDs) and SR-BI immunostaining and expression followed the same trend. Addition of HDL or PDGF partially restore the proliferation rate and significantly increase SR-BI and pAKT expression in serum-deprived cells. In conclusion, cell transition from G0 to G1/S requires CE-HDL uptake, leading to CE-HDL/SR-BI pathway activation and CEs increase into LDs.
Fabrizio Angius; Stefano Spolitu; Sabrina Uda; Stefania Deligia; Alessandra Frau; Sebastiano Banni; Maria Collu; Simonetta Accossu; Clelia Madeddu; Roberto Serpe; Barbara Batetta. High-density lipoprotein contribute to G0-G1/S transition in Swiss NIH/3T3 fibroblasts. Scientific Reports 2015, 5, 17812 .
AMA StyleFabrizio Angius, Stefano Spolitu, Sabrina Uda, Stefania Deligia, Alessandra Frau, Sebastiano Banni, Maria Collu, Simonetta Accossu, Clelia Madeddu, Roberto Serpe, Barbara Batetta. High-density lipoprotein contribute to G0-G1/S transition in Swiss NIH/3T3 fibroblasts. Scientific Reports. 2015; 5 (1):17812.
Chicago/Turabian StyleFabrizio Angius; Stefano Spolitu; Sabrina Uda; Stefania Deligia; Alessandra Frau; Sebastiano Banni; Maria Collu; Simonetta Accossu; Clelia Madeddu; Roberto Serpe; Barbara Batetta. 2015. "High-density lipoprotein contribute to G0-G1/S transition in Swiss NIH/3T3 fibroblasts." Scientific Reports 5, no. 1: 17812.
Rhinovirus infections do not only cause common colds, but may also trigger severe exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Even though rhinoviruses have been the focus of extensive drug development efforts in the past, an anti-rhinoviral drug still has to make it to the market. In the past, the viral capsid protein VP1 has been shown to be an important target for the development of antiviral molecules. Furthermore, many different chemical scaffolds appear to possess the properties that are required to inhibit virus replication by this mechanism of action. I-6602, an analogue of the rhinovirus inhibitor pirodavir, was previously identified as a potent inhibitor of rhinovirus infection. Here, we describe the antiviral activity of its analogue ca603, a molecule with a modified linker structure, and corroborate its mechanism of action as a capsid binder. The molecule ca603 shows antiviral activity against a panel of rhino-and enteroviruses. Cross-resistance is observed against viruses with mutations that render them resistant to the inhibitory effect of the capsid binder pleconaril and thermostability assays demonstrate that the compound binds and stabilizes the viral capsid. Binding of the molecule to the VP1 protein is corroborated by in silico modeling. It is confirmed that ca603 inhibits rhinovirus replication by interaction with the VP1 protein and, by this, allows to further expand the chemical diversity of capsid-binding molecules.
Céline Lacroix; SamuelA Laconi; Fabrizio Angius; Antonio Coluccia; Romano Silvestri; Raffaello Pompei; Johan Neyts; Pieter Leyssen. In vitro characterisation of a pleconaril/pirodavir-like compound with potent activity against rhinoviruses. Virology Journal 2015, 12, 1 -6.
AMA StyleCéline Lacroix, SamuelA Laconi, Fabrizio Angius, Antonio Coluccia, Romano Silvestri, Raffaello Pompei, Johan Neyts, Pieter Leyssen. In vitro characterisation of a pleconaril/pirodavir-like compound with potent activity against rhinoviruses. Virology Journal. 2015; 12 (1):1-6.
Chicago/Turabian StyleCéline Lacroix; SamuelA Laconi; Fabrizio Angius; Antonio Coluccia; Romano Silvestri; Raffaello Pompei; Johan Neyts; Pieter Leyssen. 2015. "In vitro characterisation of a pleconaril/pirodavir-like compound with potent activity against rhinoviruses." Virology Journal 12, no. 1: 1-6.
Fabrizio Angius; Maria Antonietta Madeddu; Raffaello Pompei. Nutritionally Variant Streptococci Interfere with Streptococcus mutans Adhesion Properties and Biofilm Formation. The new microbiologica 2015, 38, 1 .
AMA StyleFabrizio Angius, Maria Antonietta Madeddu, Raffaello Pompei. Nutritionally Variant Streptococci Interfere with Streptococcus mutans Adhesion Properties and Biofilm Formation. The new microbiologica. 2015; 38 (2):1.
Chicago/Turabian StyleFabrizio Angius; Maria Antonietta Madeddu; Raffaello Pompei. 2015. "Nutritionally Variant Streptococci Interfere with Streptococcus mutans Adhesion Properties and Biofilm Formation." The new microbiologica 38, no. 2: 1.
Human Herpesvirus 8 (HHV8), the causative agent of Kaposi’s sarcoma, induces an intense modification of lipid metabolism and enhances the angiogenic process in endothelial cells. In the present study, neutral lipid (NL) metabolism and angiogenesis were investigated in HHV8-infected HUVEC cells. The viral replication phases were verified by rtPCR and also by K8.1 and LANA immunostaining. Lipid droplets (Nile Red) were higher in all phases and NL staining (LipidTOX) combined with viral-antigen detection (immunofluorescence) demonstrated a NL content increase in infected cells. In particular, triglyceride synthesis increases in the lytic phase, whereas cholesteryl ester synthesis rises in the latent one. Moreover, the inhibition of cholesterol esterification reduces neo-tubule formation mainly in latently infected cells. We suggest that a reprogramming of cholesteryl ester metabolism is involved in regulating neo-angiogenesis in HHV8-infected cells and plays a likely role in the high metastatic potential of derived-tumours.
Fabrizio Angius; Sabrina Uda; Enrica Piras; Stefano Spolitu; Angela Ingianni; Barbara Batetta; Raffaello Pompei. Neutral lipid alterations in Human Herpesvirus 8-infected HUVEC cells and their possible involvement in neo-angiogenesis. BMC Microbiology 2015, 15, 1 -10.
AMA StyleFabrizio Angius, Sabrina Uda, Enrica Piras, Stefano Spolitu, Angela Ingianni, Barbara Batetta, Raffaello Pompei. Neutral lipid alterations in Human Herpesvirus 8-infected HUVEC cells and their possible involvement in neo-angiogenesis. BMC Microbiology. 2015; 15 (1):1-10.
Chicago/Turabian StyleFabrizio Angius; Sabrina Uda; Enrica Piras; Stefano Spolitu; Angela Ingianni; Barbara Batetta; Raffaello Pompei. 2015. "Neutral lipid alterations in Human Herpesvirus 8-infected HUVEC cells and their possible involvement in neo-angiogenesis." BMC Microbiology 15, no. 1: 1-10.
The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay is commonly used to evaluate the cytotoxicity potential of drugs vehicled by liposomes. However, liposome delivering drugs could produce inconsistent values of MTT absorbance. On the basis of previous experiments demonstrating the MTT affinity for lipid droplets, this paper aims to show that empty-liposomes interfere, per se, on MTT assay due to its lipidic nature. This brings into question the use of MTT testing cytotoxicity when liposomes are involved in delivering drugs.
Fabrizio Angius; Alice Floris. Liposomes and MTT cell viability assay: An incompatible affair. Toxicology in Vitro 2015, 29, 314 -319.
AMA StyleFabrizio Angius, Alice Floris. Liposomes and MTT cell viability assay: An incompatible affair. Toxicology in Vitro. 2015; 29 (2):314-319.
Chicago/Turabian StyleFabrizio Angius; Alice Floris. 2015. "Liposomes and MTT cell viability assay: An incompatible affair." Toxicology in Vitro 29, no. 2: 314-319.
F. Angius; S. Uda; S. Spolitu; S. Deligia; S. Accossu; A. Frau; B. Batetta. Inhibition of cholesterol esterification increases cholesteryl ester uptake from hdl in parental and mdr1 resistant ccrf-cem cells. Atherosclerosis 2014, 235, e301 .
AMA StyleF. Angius, S. Uda, S. Spolitu, S. Deligia, S. Accossu, A. Frau, B. Batetta. Inhibition of cholesterol esterification increases cholesteryl ester uptake from hdl in parental and mdr1 resistant ccrf-cem cells. Atherosclerosis. 2014; 235 (2):e301.
Chicago/Turabian StyleF. Angius; S. Uda; S. Spolitu; S. Deligia; S. Accossu; A. Frau; B. Batetta. 2014. "Inhibition of cholesterol esterification increases cholesteryl ester uptake from hdl in parental and mdr1 resistant ccrf-cem cells." Atherosclerosis 235, no. 2: e301.
The aim of this study was to highlight the main features of magnetoliposomes prepared by TLE, using hydrophobic magnetite, and stabilized with oleic acid, instead of using the usual hydrophilic magnetite surrounded by sodium citrate. These biocompatible magnetoliposomes (MLs) were prepared with the purpose of producing a magnetic carrier capable of loading either hydrophilic or lipophilic drugs. The effect of different liposome/magnetite weight ratios on the stability of magnetoliposomes was evaluated by monitoring the mean diameter of the particles, their polydispersity index, and zeta potential over time. The prepared magnetoliposomes showed a high liposome-magnetite association, with magnetoliposomes containing PEG (polyethylene glycol) showing the best magnetite loading values. To verify the position of magnetite nanoparticles in the vesicular structures, the morphological characteristics of the structures were studied using transmission electron microscopy (TEM). TEM studies showed a strong affinity between hydrophobic magnetite nanoparticles, the surrounding oleic acid molecules, and phospholipids. Furthermore, the concentration above which one would expect to find a cytotoxic effect on cells as well as morphological cell-nanoparticle interactions was studied in situ by using the trypan blue dye exclusion assay, and the Prussian Blue modified staining method
Alice Floris; Chiara Sinico; Anna Maria Fadda; Francesco Lai; Francesca Marongiu; Alessandra Scano; Martina Pilloni; Fabrizio Angius; Carlos Vázquez-Vázquez; Guido Ennas. Characterization and cytotoxicity studies on liposome–hydrophobic magnetite hybrid colloids. Journal of Colloid and Interface Science 2014, 425, 118 -127.
AMA StyleAlice Floris, Chiara Sinico, Anna Maria Fadda, Francesco Lai, Francesca Marongiu, Alessandra Scano, Martina Pilloni, Fabrizio Angius, Carlos Vázquez-Vázquez, Guido Ennas. Characterization and cytotoxicity studies on liposome–hydrophobic magnetite hybrid colloids. Journal of Colloid and Interface Science. 2014; 425 ():118-127.
Chicago/Turabian StyleAlice Floris; Chiara Sinico; Anna Maria Fadda; Francesco Lai; Francesca Marongiu; Alessandra Scano; Martina Pilloni; Fabrizio Angius; Carlos Vázquez-Vázquez; Guido Ennas. 2014. "Characterization and cytotoxicity studies on liposome–hydrophobic magnetite hybrid colloids." Journal of Colloid and Interface Science 425, no. : 118-127.
Increasing evidence indicates that carcinogenesis is dependent on the tissue context in which it occurs, implying that the latter can be a target for preventive or therapeutic strategies. We tested the possibility that re-normalizing a senescent, neoplastic-prone tissue microenvironment would exert a modulatory effect on the emergence of neoplastic disease. Rats were exposed to a protocol for the induction of hepatocellular carcinoma (HCC). Using an orthotopic and syngeneic system for cell transplantation, one group of animal was then delivered 8 million normal hepatocytes, via the portal circulation. Hepatocytes transplantation resulted in a prominent decrease in the incidence of both pre-neoplastic and neoplastic lesions. At the end of 1 year 50% of control animals presented with HCC, while no HCC were observed in the transplanted group. Extensive hepatocyte senescence was induced by the carcinogenic protocol in the host liver; however, senescent cells were largely cleared following infusion of normal hepatocytes. Furthermore, levels of Il-6 increased in rats exposed to the carcinogenic protocol, while they returned to near control values in the group receiving hepatocyte transplantation. These results support the concept that strategies aimed at normalizing a neoplastic-prone tissue landscape can modulate progression of neoplastic disease.
Fabio Marongiu; Maria Paola Serra; Marcella Sini; Fabrizio Angius; Ezio Laconi. Clearance of senescent hepatocytes in a neoplastic-prone microenvironment delays the emergence of hepatocellular carcinoma. Aging 2014, 6, 26 -34.
AMA StyleFabio Marongiu, Maria Paola Serra, Marcella Sini, Fabrizio Angius, Ezio Laconi. Clearance of senescent hepatocytes in a neoplastic-prone microenvironment delays the emergence of hepatocellular carcinoma. Aging. 2014; 6 (1):26-34.
Chicago/Turabian StyleFabio Marongiu; Maria Paola Serra; Marcella Sini; Fabrizio Angius; Ezio Laconi. 2014. "Clearance of senescent hepatocytes in a neoplastic-prone microenvironment delays the emergence of hepatocellular carcinoma." Aging 6, no. 1: 26-34.