A5054554528- Liver Disease Diagnosis and Treatment
- Liver physiology and pathology
- Immune Cell Function and Interaction
- Endoplasmic Reticulum Stress and Disease
- Advanced Glycation End Products research
- Liver Disease and Transplantation
- IL-33, ST2, and ILC Pathways
- Asthma and respiratory diseases
- Eosinophilic Esophagitis
- Genomics, phytochemicals, and oxidative stress
- Diabetes and associated disorders
- Diet, Metabolism, and Disease
- TGF-β signaling in diseases
- Tissue Engineering and Regenerative Medicine
- Alcohol Consumption and Health Effects
- Ferroptosis and cancer prognosis
- Hepatitis C virus research
- Connective Tissue Growth Factor Research
- Drug Transport and Resistance Mechanisms
- Hepatitis B Virus Studies
- Organ Transplantation Techniques and Outcomes
- GDF15 and Related Biomarkers
- Phagocytosis and Immune Regulation
- Diet and metabolism studies
- Immune cells in cancer
Dongguan People’s Hospital
2024-2025
Guangdong Medical College
2024
Stanford University
2020-2024
Heidelberg University
2024
Heidelberg University
2024
University Hospital Heidelberg
2024
Chinese Academy of Sciences
2016-2024
Center for Excellence in Molecular Cell Science
2019-2024
University of Chinese Academy of Sciences
2018-2023
Vision Technology (United States)
2023
Abstract Type 2 diabetes mellitus is a major risk factor for hepatocellular carcinoma (HCC). Changes in extracellular matrix (ECM) mechanics contribute to cancer development 1,2 , and increased stiffness known promote HCC progression cirrhotic conditions 3,4 . characterized by an accumulation of advanced glycation end-products (AGEs) the ECM; however, how this affects non-cirrhotic unclear. Here we find that, patients animal models, AGEs changes collagen architecture enhance ECM...
Hepatocyte ferroptosis promotes the pathogenesis and progression of liver fibrosis. Salvianolic acid B (Sal B) exerts antifibrotic effects. However, pharmacological mechanism target has not yet been fully elucidated. In this study, fibrosis was induced by CCl4 in wild-type mice hepatocyte-specific extracellular matrix protein 1 (Ecm1)-deficient mice, which were separately treated with Sal B, ferrostatin-1, sorafenib or cilengitide. Erastin- CCl4-induced hepatocyte models without Ecm1 gene...
Inflammatory bowel disease (IBD) comprises chronic relapsing disorders of the gastrointestinal tract characterized pathologically by intestinal inflammation and epithelial injury. Here, we uncover a function extracellular matrix protein 1 (ECM1) in promoting pathogenesis human mouse IBD. ECM1 was highly expressed macrophages, particularly tissue-infiltrated macrophages under inflammatory conditions, expression significantly induced during IBD progression. The macrophage-specific knockout...
Activation of TGFB (transforming growth factor β) promotes liver fibrosis by activating hepatic stellate cells (HSCs), but the mechanisms activation are not clear. We investigated role ECM1 (extracellular matrix protein 1), which interacts with extracellular and structural proteins, in mouse livers.We performed studies C57BL/6J mice (controls), ECM1-knockout (ECM1-KO) mice, hepatocyte-specific knockout EMC1 (ECM1Δhep). or soluble TGFBR2 (TGFB receptor 2) were expressed livers after injection...
Type 2 diabetes is clinically associated with progressive necroinflammation and fibrosis in nonalcoholic steatohepatitis (NASH). Advanced glycation end-products (AGEs) accumulate during prolonged hyperglycemia, but the mechanistic pathways that lead to accelerated liver have not been well defined. In this study, we show AGEs clearance receptor AGER1 was downregulated patients NASH our models, whereas proinflammatory RAGE induced. These findings were necroinflammatory, fibrogenic, pro-oxidant...
Ulcerative colitis (UC) is non-specific inflammatory bowel disease. UC development and progression were closely associated with epigenetic modifications. Nevertheless, the specific relationship between N6-methyladenosine (m6A) modification at RNA transcription levels pathogenesis remains unclear. We established cell models mouse through dextran sulfate sodium (DSS) induction. The expression of METTL14 analyzed via qRT-PCR western blot. In vitro functional experiments evaluated effects...
T-follicular helper (TFH) cells are a subset of CD4+ T that help germinal center (GC) B-cell differentiation and high-affinity antibody production during reactions. Whether important extracellular molecules control TFH is not fully understood. Here, we demonstrate secreted protein matrix 1 (ECM1) critical for response. A lack ECM1 inhibited cell development impaired GC reactions antigen-specific in an antigen-immunized mouse model. was induced by IL-6 IL-21 cells, promoting down-regulating...
The recently discovered interferon lambda 4 (IFN-λ4) is a new member of the human type III interferons which could induce strong antiviral effect through JAK–STAT cascade. However, hepatitis C virus (HCV) patients who are capable expressing IFN-λ4 usually have poor response to IFN-α treatment, and mechanism behind this paradox remains unknown. Here, we reported that desensitized IFN-α-stimulated signalling. Microarray analysis revealed ubiquitin specific peptidase 18 (USP18), known inhibitor...
Background and Aims Older patients with obesity/type II diabetes mellitus frequently present advanced NASH. Whether this is due to specific molecular pathways that accelerate fibrosis during aging unknown. Activation of the Src homology 2 domain–containing collagen‐related (Shc) proteins redox stress have been recognized in aging; however, their link NASH has not explored. Approach Results Shc expression increased livers older NASH, as assessed by real time quantitative PCR (RT‐qPCR) or...
Induction of broadly neutralizing monoclonal antibodies (bNAbs) that bind to the viral envelope glycoproteins is a major goal hepatitis C virus (HCV) vaccine research. The study bNAbs arising in natural infection essential this endeavor. We generated human antibody, 8D6, recognizing E2 protein HCV isolated from chronic patient. This antibody shows activity, which covers pan-genotypic panel cell culture-derived virions (HCVcc). Functional and epitope analyses demonstrated 8D6 can block...
Objective: Extracellular Matrix Protein 1 (ECM1) serves as a gatekeeper of hepatic fibrosis by maintaining transforming growth factor-β1 (TGF-β1) in its latent form. ECM1 knockout (KO) causes (L) TGF-β1 activation, resulting with rapid mortality. In chronic liver disease (CLD), decreases increasing CLD severity. We investigate the regulatory role bioavailability and impact on progression. Design: RNAseq was performed to analyze gene expression. Functional assays were using stellate cells...
Chronic Liver Disease (CLD) is characterized by progressive liver fibrosis, where the dysregulation of transforming growth factor-β 1 (TGF-β1) activation plays a pivotal role. Our study investigates mechanism extracellular matrix protein (ECM1) in modulating LTGF-β1 bioactivity and its impact on CLD progression.
In healthy liver, latent TGF-β is stored in the extracellular matrix and kept quiescent by ECM1. Upon damage, ECM1 production downregulated hepatocytes leading to L-TGF-β activation, thus inducing HSC activation subsequent liver injuries. This study investigates underlying regulatory mechanism of expression under different pathophysiological conditions. Physiologically, maintained EGF/EGFR/STAT1 pathway. Blocking EGFR significantly inhibits both vitro vivo. Knockdown Stat1 sufficient...
Abstract In healthy livers, extracellular matrix protein 1 (ECM1) is essential for liver homeostasis by keeping latent transforming growth factor-β (LTGF-β) quiescent. Upon hepatocyte damage, ECM1 downregulated, facilitating LTGF-β activation and fibrogenesis. However, little known about how hepatic regulated. Here we found in hepatocytes, EGF/EGFR signaling sustains expression through phosphorylating STAT1 at S727, enhancing its binding to the promoter boosting gene transcription. During...