Objective(s): Long noncoding RNAs (lncRNAs)-activated by transforming growth factor beta (lncRNA-ATB) is known to be involved in the invasion of hepatocellular carcinoma by regulating target genes of miR-200a. However, the role and molecular mechanisms of lncRNA-ATB/miR-200a in HCV-related liver fibrosis remains unclear. In this study, we examined the expression of lncRNA-ATB/miR-200a, and their target gene β-Catenin in liver tissues of HCV patients and hepatic stellate cells (HSCs) to elucidate the possible role of lncRNA-ATB/miR-200a axis in HSC activation and development of liver fibrosis.
Materials And Methods: Liver tissues were obtained by biopsy or surgery from eighteen HCV patients with severe liver fibrosis and six healthy subjects (control). Conditioned media (CM) from cultured HepG2-CORE cells (HepG2 cells stably expressing HCV core protein) were used to treat LX-2 cells. The binding sites between lncRNA-ATB/miR-200a and β-catenin were predicted and then verified by a dual luciferase reporter assay. The effect of lncRNA-ATB/miR-200a/β-catenin on HSC activation was assessed by examining the expression of alpha-smooth muscle actin (α-SMA) and collagen type 1 alpha 1 (Col1A1) in HSCs. Further, the regulatory role of lncRNA-ATB on HSC activation and miR-200a/β-catenin expression was assessed by using siRNA-mediated knockdown of lncRNA-ATB.
Results: LncRNA-ATB was up-regulated in fibrotic liver tissues and activated LX-2 cells treated with CM from HepG2-CORE cells. Dual luciferase reporter assays confirmed that lncRNA-ATB contained common binding sites for miR-200a and β-catenin. Decreased expression of miR-200a and increased expression of β-catenin were observed in liver tissues of patients with HCV-related hepatic fibrosis and activated HSCs. Knockdown of lncRNA-ATB could down-regulate β-catenin expression by up-regulating the endogenous miR-200a and suppress the activation of LX-2 cells.
Conclusion: LncRNA-ATB/miR-200a/β-catenin regulatory axis likely contributed to the development of liver fibrosis in HCV patients. Knockdown of lncRNA-ATB might be a novel therapeutic target for HCV-related liver fibrosis.
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http://dx.doi.org/10.1016/j.gene.2017.03.008 | DOI Listing |
Curr Obes Rep
January 2025
Dipartimento Psicologia e Scienze della Salute, Università Telematica Pegaso, Centro Direzionale Isola F2, Via Porzio, Naples, 80143, Italy.
Purpose Of Review: This narrative review explores the role of Medical Nutritional Therapy (MNT) in managing Metabolic-Associated Steatotic Liver Disease (MASLD), previously known as nonalcoholic fatty liver disease. It aims to examine the effectiveness of specific nutritional strategies in preventing and treating this obesity-linked liver disease.
Recent Findings: Emerging evidence underscores the benefits of the Mediterranean diet, low-carbohydrate diets, and intermittent fasting in reducing liver fat, improving insulin sensitivity, and mitigating inflammation.
Background: The mechanism underlying chronic drug-induced liver injury (DILI) remains unclear. Immune activation is a common feature of DILI progression and is closely associated with metabolism. We explored the immunometabolic profile of chronic DILI and the potential mechanism of chronic DILI progression.
View Article and Find Full Text PDFBMJ Open Gastroenterol
December 2024
Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
Objective: Preventing return to alcohol is of critical importance for patients with alcohol-related cirrhosis and/or alcohol-associated hepatitis. Acamprosate is a widely used treatment for alcohol use disorder (AUD). We assessed the impact of acamprosate prescription in patients with advanced liver disease on abstinence rates and clinical outcomes.
View Article and Find Full Text PDFBMJ Open Gastroenterol
December 2024
Australian Centre for Health Services Innovation, Centre for Healthcare Transformation, School of Public Health and Social Work, Faculty of Health, Queensland University of Technology, Kelvin Grove, Queensland, Australia
Objective: Non-alcoholic fatty liver disease (NAFLD) is estimated to affect a third of Australian adults, and its prevalence is predicted to rise, increasing the burden on the healthcare system. The LOCal Assessment and Triage Evaluation of Non-Alcoholic Fatty Liver Disease (LOCATE-NAFLD) trialled a community-based fibrosis assessment service using FibroScan to reduce the time to diagnosis of high-risk NAFLD and improve patient outcomes.
Methods: We conducted a 1:1 parallel randomised trial to compare two alternative models of care for NAFLD diagnosis and assessment.
Aliment Pharmacol Ther
January 2025
Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California, USA.
Our study investigated the prevalence of lean steatotic liver disease (SLD) and its subcategories, including metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-related and alcohol-related SLD (MetALD), and alcohol-related liver disease (ALD) among lean adults in the US. Analysing data from 2965 lean adults (≥ 18 years) from the National Health and Nutrition Examination Survey (2017-2023), we found the age-adjusted prevalence of lean SLD to be 12.8%.
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