Hydrostatic pressure induces profibrotic properties in hepatic stellate cells via the RhoA/ROCK signaling pathway. Issue 6 (15th April 2022)

• Record Type: Journal Article
• Authors: Huang, Zisheng; Khalifa, Mahmoud Osman; Gu, Weili; Li, Tao‐Sheng
• Other Names: López‐Lastra Marcelo guestEditor.
• Is Part Of: FEBS open bio. Volume 12:Issue 6(2022)
• Page Start: 1230
• Page End: 1240
• Publication Date: 2022-04-15
• Subjects: hepatic stellate cells -- hydrostatic pressure -- liver fibrosis -- mechanotransduction -- RhoA/ROCK; Molecular biology -- Periodicals; Cytology -- Periodicals; Life sciences -- Periodicals; Biological Science Disciplines -- Periodicals; Molecular Biology -- Periodicals; Cell Biology -- Periodicals; Cytology; Life sciences; Molecular biology; Periodicals; 572.805
• DOI: 10.1002/2211-5463.13405
• Languages: English
• ISSNs: 2211-5463

Abstract

Abstract : Elevated interstitial fluid hydrostatic pressure is commonly observed in diseased livers. We herein examined the hypothesis that hydrostatic pressure induces hepatic stellate cells to acquire profibrotic properties under pathological conditions. Human hepatic stellate cells were exposed to 50 mmHg pressure for 24 h. Although we observed few changes of cell growth and morphology, PCR array data on the expression of fibrosis‐associated genes suggested the acquisition of profibrotic properties. The exposure of hepatic stellate cells to 50 mmHg pressure for 24 h also significantly enhanced the expression of RhoA, ROCK1, α‐SMA, TGF‐β1, p‐MLC, and p‐Smad2, and this was effectively attenuated by the ROCK inhibitor Y‐27632. Our ex vivo experimental data suggest that elevated interstitial fluid hydrostatic pressure under pathological conditions may promote liver fibrosis by inducing acquisition of profibrotic properties of hepatic stellate cells through the RhoA/ROCK signaling pathway. Abstract : In this study we demonstrated that elevated fluid hydrostatic pressure under pathological conditions may subsequently promote liver fibrosis by activating hepatic stellate cells through the RhoA/ROCK signaling pathway, providing a possible target for preventing fibrosis progression.