Screening of differentially expressed miRNAs in tensile strain‑treated HepG2 cells by miRNA microarray analysis.

Cirrhosis and portal hypertension are associated with an increased risk of developing liver cancer. However, it is unknown how changes in the cellular mechanical microenvironment induced by portal hypertension affect the occurrence and development of liver cancer. The aim of this study was to determine the effect of tensile strain on the proliferation of a human liver cancer cell line (HepG2 cells) using methods such as flow cytometry, Cell Counting Kit‑8 and 5‑bromodeoxyuridine assays, and to examine the changes in microRNA (miRNA/miR) expression using microarray, reverse transcription‑quantitative (RT‑q)PCR and bioinformatics analyses.

Identification of miRNAs associated with the mechanical response of hepatic stellate cells by miRNA microarray analysis.

It has been suggested that hepatic stellate cells (HSCs) could be used in the regulation of liver microcirculation and portal hypertension. The effects of tensile strain on the microRNA (miRNA) profile of HSCs are largely unknown. In this study, we aimed to explore the changes of miRNA expression in tensile strain-treated HSCs.

Mechanical force and tensile strain activated hepatic stellate cells and inhibited retinol metabolism.

Objectives: Hepatic stellate cells (HSCs), the principal producers of extracellular matrix proteins, play a major role in the development of liver fibrosis which is accompanied with elevated sinusoidal pressure and portal hypertension. We have isolated primary rat HSCs and investigated the effect of mechanical pressure and tensile strain on retinol metabolism in the cells.

Results: Mechanical force and tensile strain significantly increased the expression of α-smooth muscle actin (α-SMA) and collagen I, and notably inhibited the expression of cellular retinol-binding protein I (CRBP-I), lecithin-retinol acyltransferase (LRAT), retinyl ester hydrolase (REH), retinoic acid receptor-β (RAR-β) and retinoid X receptor-α (RXR-α).