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Seven Steps to Stellate Cells

Seven Steps to Stellate Cells

Published on: May 10, 2011

The miR-23b/27b/24-1 Cluster Inhibits Hepatic Fibrosis by Inactivating Hepatic Stellate Cells.

Lin-Yan Wan¹, Hu Peng², Yi-Ran Ni³

¹Medical College, Yichang, China; Institute of Organ Fibrosis and Targeted Drug Delivery, Yichang, China; Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, Yichang, China; State Key Laboratory of Medical Molecular Biology, Department of Physiology, Institute of Basic Medical Sciences, School of Basic Medicine, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China; Institute of Organ Fibrosis and Targeted Drug Delivery, The People's Hospital, China Three Gorges University, Yichang, China.

Cellular and Molecular Gastroenterology and Hepatology

|January 30, 2022

Summary

The microRNA-23b/27b/24-1 cluster can inhibit hepatic stellate cell activation and reduce extracellular matrix deposition, offering a potential new treatment for liver fibrosis.

Keywords:

Gremlin1 Hepatic Fibrosis Hepatic Stellate Cells Itgα2/5 LOX TGF-β2 miR-23b/27b/24-1 Cluster

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Murine Precision-Cut Liver Slices as an Ex Vivo Model of Liver Biology

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Published on: March 14, 2020

Area of Science:

Molecular Biology
Hepatology
Biochemistry

Background:

Hepatic fibrosis, a precursor to cirrhosis, involves hepatic stellate cell (HSC) activation and extracellular matrix (ECM) deposition.
Current antifibrotic therapies are limited, highlighting the need for novel therapeutic strategies.

Purpose of the Study:

To investigate the antifibrotic potential of the microRNA-23b/27b/24-1 cluster in hepatic fibrosis.
To elucidate the molecular mechanisms by which this microRNA cluster impacts HSC activation and ECM production.

Main Methods:

Carbon tetrachloride (CCl4)-induced liver fibrosis model in C57BL/6 mice treated with miR-23b/27b/24-1 lentivirus.
Primary rat HSC and HSC-T6 cell lines were used for mechanistic studies.
Techniques included RNA-sequencing, luciferase reporter assays, western blotting, and bioinformatics analysis.

Main Results:

Intravenous delivery of miR-23b/27b/24-1 lentivirus ameliorated liver fibrosis in mice.
The cluster directly targeted mRNAs, reducing protein expression of profibrotic factors (TGF-β2, Gremlin1, LOX, Itgα2, Itgα5) in HSCs.
This led to suppression of TGF-β signaling, activation of bone morphogenetic protein signaling, reduced ECM secretion, ECM softening, and increased ECM degradation.

Conclusions:

Hepatic overexpression of the miR-23b/27b/24-1 cluster effectively blocked liver fibrosis in a mouse model.
This microRNA cluster represents a promising novel therapeutic approach for patients suffering from hepatic fibrosis.