Aixia Zhai

Prof. Aixia Zhai


Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 March 2020 in Molecular Therapy Nucleic Acids
Verified
Journal Article
Open access
BLBo Li
Bo Li
SLSong Luan
Song Luan
JCJing Chen
Jing Chen
YZYue Zhou
Yue Zhou
TWTingting Wang
Tingting Wang
CBChanglong Bi
Changlong Bi
Mesenchymal stem cells (MSCs) have been reported to hold promise to accelerate the wound-healing process in diabetic foot ulcer (DFU) due to the multilineage differentiation potential. Hence, this study intended to explore the wound healing role of MSC-derived exosomes containing long noncoding RNA (lncRNA) H19 in DFU. lncRNA H19 was predicated to bind to microRNA-152-3p (miR-152-3p), which targeted phosphatase and tensin homolog (PTEN) deleted on chromosome ten. Fibroblasts in DFU samples exhibited highly expressed miR-152-3p and poorly expressed lncRNA H19 and PTEN, along with an activated phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt1) signaling pathway. The fibroblasts were cocultured with lncRNA H19-transfected MSCs and MSC-derived exosomes to assess the effect of the lncRNA H19/miR-152-3p/PTEN axis on the biological activities and inflammation in fibroblasts. Mouse models of DFU were developed by streptozotocin, which was injected with MSC-derived exosomes overexpressing lncRNA H19. lncRNA H19 in MSCs was transferred through exosomes to fibroblasts, the mechanism of which improved wound healing in DFU, corresponded to promoted fibroblast proliferation and migration, as well as suppressed apoptosis and inflammation. Wound healing in mice with DFU was facilitated following the injection of MSC-derived exosomes overexpressing lncRNA H19. Taken together, MSC-derived exosomal lncRNA H19 prevented the apoptosis and inflammation of fibroblasts by impairing miR-152-3p-mediated PTEN inhibition, leading to the stimulated wound-healing process in DFU.

10 November 2020 in The FASEB Journal
Verified
Journal Article
Open access
PDF file
BLBo Li
Bo Li
YZYue Zhou
Yue Zhou
JCJing Chen
Jing Chen
TWTingting Wang
Tingting Wang
ZLZhijuan Li
Zhijuan Li
CBChanglong Bi
Changlong Bi
Aberrant expression of long noncoding RNA (lncRNA) H19 and microRNA (miR)‐29b has been implicated in the complications of diabetes mellitus (DM). As a common and important complication of DM, diabetic foot ulcer (DFU) is characterized by high incidence and poor prognosis. Herein, we explored the role of lncRNA H19 in wound healing of DFU. Differentially expressed DM‐related lncRNAs were initially screened by microarray data analysis. DFU models were then induced in DM mouse models. The functional role and interaction of lncRNA H19, miR‐29b and FBN1 in DFU were subsequently determined by examining the proliferation, migration, and apoptosis of fibroblasts after silencing H19, inhibiting or overexpressing miR‐29b and FBN1. According to microarray‐based analysis, lncRNA H19 was upregulated in DM. In the ulcerative edge tissues of DFU, high expression of lncRNA H19 and FBN1 and low expression of miR‐29b were observed. FBN1 was identified to be a target gene of miR‐29b. LncRNA H19 could competitively bind to miR‐29b, and then, inhibited its expression, which consequently upregulating FBN1. Silencing of lncRNA H19 led to inhibited proliferation, migration, and enhanced apoptosis of fibroblasts, accompanied by downregulated FBN1 but upregulated miR‐29b, which diminished the expression of TGF‐β1, Smad3, FN, and Col‐1 and reduced extracellular matrix accumulation. Altogether, upregulation of lncRNA H19 can elevate the expression of FBN1 through competitively binding to miR‐29b, which enhances the proliferation, migration, and inhibits apoptosis of fibroblasts, thus facilitating the wound healing of DFU.

24 November 2022 in Frontiers in Microbiology
Verified
Journal Article
Open access
XYXin Yu
Xin Yu
YCYing Chen
Ying Chen
LCLele Cui
Lele Cui
KYKaming Yang
Kaming Yang
XWXumeng Wang
Xumeng Wang
AZAixia Zhai
Aixia Zhai
Background: Chronic hepatitis B (CHB) remains a significant global health problem, leading to recurrent inflammation and liver-damaging diseases such as fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Currently, although diagnostic markers for CHB are well established, the indicators for predicting liver injury caused by hepatitis B virus (HBV) infection still need to be further explored. Thus, the identification of credible infectious indicators is urgently needed to facilitate timely clinical intervention and avoid the progression of disease malignancy.Methods: The Gene Expression Omnibus (GEO) database GSE83148 data set was used to explore the hub genes for HBV infection. The quantitative real-time polymerase chain reaction (qPCR) was used to identify the impact of HBV infection on the expression of hub gene at the cell level. At the same time, serum samples and clinical information were collected from healthy, HBV-free and CHB patients. The enzyme-linked immunosorbent assay (ELISA) was used to verify the results of cell experiments and Pearson correlation analysis was used to clarify hub genes correlation with HBV infection indicators and liver injury-related indicators. Finally, the Gene Expression Profiling Interactive Analysis (GEPIA) database was used to analyze the differences in the expression of hub gene in liver injury diseases.Results: Chemokine (C-X-C motif) ligand (CXCL)8, CXCL9, CXCL10, and CXCL11 were identified as hub genes in HBV infection. After HBV infection, the expression of the four chemokines was significantly increased and the concentrations secreted into serum were also increased. Moreover, the four chemokines were significantly correlated with HBV infection-related indicators and liver injury-related indicators, which were positively correlated with alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hepatitis B e antigen (HBeAg), and negatively correlated with AST/ALT ratio and hepatitis B core antibody (HBcAb). In addition, the expression of CXCL9, CXCL10, and CXCL11 in HCC tissues was significantly higher than in normal tissues.Conclusion: Using a combination of bioinformatics, cell experiments, and clinical correlation analysis, this study showed that CXCL8, CXCL9, CXCL10, and CXCL11 can be used as serum biomarkers to forecast liver injury caused by HBV infection.

10 April 2024 in Journal of Diabetes
Verified
Journal Article
Open access
YLYuetong Li
Yuetong Li
YLYuxin Leng
Yuxin Leng
YLYang Liu
Yang Liu
JZJianhua Zhong
Jianhua Zhong
JLJiaxin Li
Jiaxin Li
AZAixia Zhai
Aixia Zhai
Aim: Hydrogels with excellent biocompatibility and biodegradability can be used as the desirable dressings for the therapy of diabetic foot ulcer (DFU). This review aimed to summarize the biological functions of hydrogels, combining with the pathogenesis of DFU.Methods: The studies in the last 10 years were searched and summarized from the online database PubMed using a combination of keywords such as hydrogel and diabetes. The biological functions of hydrogels and their healing mechanism on DFU were elaborated.Results: In this review, hydrogels were classified by their active substances such as drugs, cytokines, photosensitizers, and biomimetic peptide. Based on this, the biological functions of hydrogels were summarized by associating the pathogenesis of DFU, including oxidative stress, chronic inflammation, cell phenotype change, vasculopathy, and infection. This review also pointed out some of the shortcomings of hydrogels in present researches.Conclusions: Hydrogels were classified into carrier hydrogels and self‐functioning hydrogels in this review. Besides, the functions and components of existing hydrogels were clarified to provide assistance for future researches and clinical applications. image

10 March 2022 in Journal of Global Antimicrobial Resistance
Verified
Journal Article
Open access
YCYing Chen
Ying Chen
XCXingchi Chen
Xingchi Chen
ZLZheng Liang
Zheng Liang
SFShuhao Fan
Shuhao Fan
XGXiaoli Gao
Xiaoli Gao
CWChao Wu
Chao Wu
Multidrug-resistant bacteria (MDRB) result in nosocomial infections and a substantial disease burden for hospitalised patients worldwide. However, strategies to control drug resistance at the hospital level are lacking. In this study, we aimed to find important indicators for risk assessment and predicting MDRB infections in the hospital. Using real-world data and machine learning models, we conducted a retrospective study from 2010 to 2020 in a teaching hospital to analyse the trends and characteristics of MDRB infections. Combining 39 hospital indicators, we used a random forest model and cross-correlation analysis to explore the important factors affecting MDRB and their predictive power. We built a decision tree model to predict the number of hospitalised patients with MDRB infection. The number of hospitalised rescues and rate of rational perioperative antibacterial drug use in type I and II incision operations were correlated with the number of patients with MDRB infection after 1-2 months. The number of hospitalised operations and rate of antibiotics use in emergency patients had an effect on current MDRB-susceptible patients. The indicators, including hospital operation volume and antibacterial drug use, had a positive or negative quantitative relationship with the number of patients with MDRB infection, and their thresholds could be fit to the MDRB prediction model. Surgical, emergency, and hospitalised rescue patients showed the highest risk of MDRB infection. Standardised indicators such as clinical pathway rate and rational antibiotic use rate could be used to control the development and spread of MDRB infections in the hospital.

18 August 2023 in Frontiers in Immunology
Verified
Journal Article
Open access
YLYang Liu
Yang Liu
GHGang Hu
Gang Hu
YLYuetong Li
Yuetong Li
XKXinyi Kong
Xinyi Kong
KYKaming Yang
Kaming Yang
AZAixia Zhai
Aixia Zhai
Cell migration–inducing protein (CEMIP), also known as KIAA1199 and hyaluronan-binding protein involved in hyaluronan depolymerization, is a new member of the hyaluronidase family that degrades hyaluronic acid (HA) and remodels the extracellular matrix. In recent years, some studies have reported that CEMIP can promote the proliferation, invasion, and adhesion of various tumor cells and can play an important role in bacterial infection and arthritis. This review focuses on the pathological mechanism of CEMIP in a variety of diseases and expounds the function of CEMIP from the aspects of inhibiting cell apoptosis, promoting HA degradation, inducing inflammatory responses and related phosphorylation, adjusting cellular microenvironment, and regulating tissue fibrosis. The diagnosis and treatment strategies targeting CEMIP are also summarized. The various functions of CEMIP show its great potential application value.