Next Article in Journal
Molecular Implications of Natriuretic Peptides in the Protection from Hypertension and Target Organ Damage Development
Previous Article in Journal
Positive Impact of Pulsed Electric Field on Lactic Acid Removal, Demineralization and Membrane Scaling during Acid Whey Electrodialysis
Article Menu
Issue 4 (February-2) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2019, 20(4), 796; https://doi.org/10.3390/ijms20040796

MicroRNA29a Reverts the Activated Hepatic Stellate Cells in the Regression of Hepatic Fibrosis through Regulation of ATPase H+ Transporting V1 Subunit C1

1
School of Pharmaceutical Science, Jiangnan University, Wuxi 214122, China
2
National Engineering Laboratory for Cereal Fermentation Technology, Jiangnan University, Wuxi 214122, China
3
The Key Laboratory of Industrial Biotechnology, Ministry of Education; School of Biotechnology, Jiangnan University, Wuxi 214122, China
*
Authors to whom correspondence should be addressed.
Received: 5 January 2019 / Revised: 7 February 2019 / Accepted: 11 February 2019 / Published: 13 February 2019
(This article belongs to the Section Molecular Biology)
Full-Text   |   PDF [3848 KB, uploaded 13 February 2019]   |  
  |   Review Reports

Abstract

Activated hepatic stellate cells (aHSCs) play a key role in liver fibrosis. During the regression of fibrosis, aHSCs are transformed into inactivated cells (iHSCs), which are quiescent lipid-containing cells and express higher levels of lipid-related genes, such as peroxisome proliferators-activated receptors gamma (PPARγ). Here, we investigated the role of MicroRNA29a (Mir29a) in the resolution of liver fibrosis. Mir29a and lipid-related genes were up-regulated after the recovery of CCl4-induced liver fibrosis in mice. PPARγ agonist rosiglitazone (RSG) promoted de-differentiation of aHSCs to iHSCs and up-regulated MIR29a expression in a human HSC cell line LX-2. MIR29a mimics in vitro promoted the expression of lipid-related genes, while decreased the expression of fibrosis-related genes. MIR29a inhibitor showed the reverse effects. ATPase H+ transporting V1 subunit C1 (Atp6v1c1) was increased in liver fibrosis, while down-regulated after the recovery in mice, and negatively regulated by MIR29a in LX-2 cells. Knockdown of ATP6V1C1 by siRNA decreased alpha-smooth muscle actin (α-SMA) and increased lipid-related genes expression. Simultaneous addition of MIR29a mimics and ATP6V1C1 siRNA further increased RSG promoted expression of lipid-related proteins in vitro. Collectively, MIR29a plays an important role during the trans-differentiation of aHSCs in the resolution of liver fibrosis, in part, through regulation of ATP6V1C1. View Full-Text
Keywords: cell differentiation; fibrosis regression; hepatic fibrosis; peroxisome proliferators-activated receptors gamma (PPARγ); vacuolar adenosine triphosphatase (V-ATPase) cell differentiation; fibrosis regression; hepatic fibrosis; peroxisome proliferators-activated receptors gamma (PPARγ); vacuolar adenosine triphosphatase (V-ATPase)
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material

SciFeed

Share & Cite This Article

MDPI and ACS Style

Jing, F.; Geng, Y.; Xu, X.-Y.; Xu, H.-Y.; Shi, J.-S.; Xu, Z.-H. MicroRNA29a Reverts the Activated Hepatic Stellate Cells in the Regression of Hepatic Fibrosis through Regulation of ATPase H+ Transporting V1 Subunit C1. Int. J. Mol. Sci. 2019, 20, 796.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top