RETRACTED: microRNA-155 Modulates Hepatic Stellate Cell Proliferation, Apoptosis, and Cell Cycle Progression in Rats With Alcoholic Hepatitis via the MAPK Signaling Pathway Through Targeting SOCS1

Abstract

The aim of this study was to investigate the regulatory function of the non-coding microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) in alcoholic hepatitis (AH) and its potential mechanism associated with the mitogen-activated protein kinase (MAPK) signaling pathway. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB), total bilirubin (TBIL), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured in a rat model of AH. The biological prediction website microRNA.org and dual-luciferase reporter gene assay were used to identify whether SOCS1 was a direct target of miR-155, and the effects of miR-155 and SOCS1 on the viability, cycle progression, and apoptosis of hepatic stellate cells were assessed using RT-qPCR, Western blot assay, MTT assay, Annexin V/PI double staining, and PI single staining. The levels of ALT, AST, MDA, and TBIL and the liver cell morphology were all prominently changed in AH model rats. miR-155 suppressed SOCS1 by specifically binding to SOCS1-3'-UTR to activate the MAPK signaling pathway. SOCS1 had low expression while miR-155 was highly expressed in AH rats. miR-155 promoted hepatic stellate cell viability and cycle progression and reduced cell apoptosis by silencing SOCS1. Together, we find that silenced miR-155 could upregulate SOCS1 and inactivate the MAPK signaling pathway, thereby inhibiting the proliferation of alcoholic hepatic stellate cells and promoting cell apoptosis.

Exosomes Derived From Hypertrophic Cardiomyocytes Induce Inflammation in Macrophages via miR-155 Mediated MAPK Pathway

“…It was previously reported that miR-155 was involved in the mediation of the MAPK signaling pathway (22). Moreover, miR-155 played a critical role in regulating inflammatory responses through the MAPK signaling pathway (23). Therefore, the present findings of intercorrelation between miR-155 and the MAPK signaling pathway in the regulation of inflammatory processes are consistent with a range of previous results in other systems.…”

Wogonoside attenuates liver fibrosis by triggering hepatic stellate cell ferroptosis through SOCS1/P53/SLC7A11 pathway

“…In response to external injurious stimul, quiescent HSCs undergo a complex activation process including downregulation of vitamin A, de novo expression of the cytoskeletal protein α‐smooth muscle actin (α‐SMA) and redundant production of ECM components such as α1(I)collagen (COL1α1), and differentiate into proliferating myofibroblast‐like cells (Kisseleva & Brenner, 2021; Pellicoro, Ramachandran, Iredale, & Fallowfield, 2014). Some tumor suppressor genes, including suppressor of cytokine signaling 1 (SOCS1) and tumor protein 53 (P53), have been found to be involved in the process of liver fibrosis (Ahsan & Mehal, 2014; Jin et al, 2016;Kandhi et al, 2016; Liu et al, 2020). Liver tissues in SOCS1‐deficient mice show increased expression of genes coding for α‐SMA, COL1α1 and enzymes involved in remodeling the ECM.…”

“…Liver tissues in SOCS1‐deficient mice show increased expression of genes coding for α‐SMA, COL1α1 and enzymes involved in remodeling the ECM. And primary HSCs from SOCS1‐deficient mice show enormous proliferative capacity in response to growth factors (Kandhi et al, 2016; Liu et al, 2020). Moreover, down‐regulation of P53 enhances the proliferation of HSC lines and primary cells, while an increase of P53 inhibits HSC proliferation (Ahsan & Mehal, 2014; Jin et al, 2016).…”

Extracellular vesicles: Natural liver‐accumulating drug delivery vehicles for the treatment of liver diseases

“…Treatments for ALF are limited to orthotopic liver transplantation and the use of artificial livers in the clinic, both of which are highly invasive. MicroRNA‐155 (miR‐155) has been shown to aggravate liver injury (Liu et al., 2020; Zhang et al., 2019). Downregulation of miR‐155 by antisense oligonucleotides (ASOs) of miR‐155 (miR155‐ASOs) was reported to alleviate septic liver injury by inhibiting oxidative stress (Yang et al., 2018), suggesting these molecules are promising therapeutic drugs for ALF.…”