Details

Autor(en) / Beteiligte

• Jing, Fei
• Geng, Yan
• Xu, Xin-Yi
• Xu, Hong-Yu
• Shi, Jin-Song
• Xu, Zheng-Hong

Titel

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

Ist Teil von

• International journal of molecular sciences, 2019-02, Vol.20 (4), p.796

Ort / Verlag

Switzerland: MDPI AG

Erscheinungsjahr

2019

Link zum Volltext

Quelle

EZB Free E-Journals

Beschreibungen/Notizen

• 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 in the resolution of liver fibrosis. 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 expression in a human HSC cell line LX-2. mimics in vitro promoted the expression of lipid-related genes, while decreased the expression of fibrosis-related genes. 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 in LX-2 cells. Knockdown of ATP6V1C1 by siRNA decreased alpha-smooth muscle actin (α- ) and increased lipid-related genes expression. Simultaneous addition of mimics and siRNA further increased RSG promoted expression of lipid-related proteins in vitro. Collectively, plays an important role during the trans-differentiation of aHSCs in the resolution of liver fibrosis, in part, through regulation of .