β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway

Objective To investigate the role ofβ-arrestin1 (ARRB1) in liver fibrosis and elucidate the mechanism of hepatic stellate cell activation induced by ARRB1/p38 signaling pathway to promote liver fibrosis. Methods Twelve male C57BJ/6L mice were randomly divided into the control (n = 6) and model group...

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Main Author: Xia Yanhao, Liu Huiling, Jiang Jie, Wu Bin
Format: Article
Language:zho
Published: Editorial Office of Journal of New Medicine 2023-01-01
Series:Xin yixue
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Online Access:https://www.xinyixue.cn/fileup/0253-9802/PDF/1676008145801-948190697.pdf
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author Xia Yanhao, Liu Huiling, Jiang Jie, Wu Bin
author_facet Xia Yanhao, Liu Huiling, Jiang Jie, Wu Bin
author_sort Xia Yanhao, Liu Huiling, Jiang Jie, Wu Bin
collection DOAJ
description Objective To investigate the role ofβ-arrestin1 (ARRB1) in liver fibrosis and elucidate the mechanism of hepatic stellate cell activation induced by ARRB1/p38 signaling pathway to promote liver fibrosis. Methods Twelve male C57BJ/6L mice were randomly divided into the control (n = 6) and model groups(n = 6). The liver fibrosis mouse model was established by 20% carbon tetrachloride. In addition, liver tissue samples from patients with liver cirrhosis and healthy controls were collected. Liver fibrosis was assessed by HE and Sirius red staining. The expression levels of ARRB1, p38, pp38, α-SMA and collagen Ⅰ were detected by immunohistochemistry, western blot and quantitative real-time PCR. The human hepatic stellate cell line LX2 was activated by TGF-β cytokine and the expression level of ARRB1 was analyzed. Furthermore, siRNA or plasmid was used to silence or overexpress ARRB1, and p38 specific inhibitor (SB203580) was adopted to reveal the regulatory relationship between ARRB1 and p38. Results ARRB1 expression was up-regulated and the activation of p38 signal was strengthened in liver fibrosis tissues(all P < 0.05). TGF-β treatment activated hepatic stellate cells and ARRB1 and p38 signaling in hepatic stellate cell LX2. The up-regulation or down-regulation of ARRB1 expression level could correspondingly affect p38 signaling and regulate the activity of hepatic stellate cells, while the change of p38 activity exerted no effect uponthe expression of ARRB1. Conclusion The expression level of ARRB1 is up-regulated in liver fibrosis, which can activate hepatic stellate cells by activating the p38 signaling, thereby promoting the incidence and development of liver fibrosis.
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spelling doaj.art-96b836c2ad5546aebfb1f735baab3c722023-02-10T06:41:47ZzhoEditorial Office of Journal of New MedicineXin yixue0253-98022023-01-01541596510.3969/j.issn.0253-9802.2023.01.013β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathwayXia Yanhao, Liu Huiling, Jiang Jie, Wu Bin0Department of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, ChinaObjective To investigate the role ofβ-arrestin1 (ARRB1) in liver fibrosis and elucidate the mechanism of hepatic stellate cell activation induced by ARRB1/p38 signaling pathway to promote liver fibrosis. Methods Twelve male C57BJ/6L mice were randomly divided into the control (n = 6) and model groups(n = 6). The liver fibrosis mouse model was established by 20% carbon tetrachloride. In addition, liver tissue samples from patients with liver cirrhosis and healthy controls were collected. Liver fibrosis was assessed by HE and Sirius red staining. The expression levels of ARRB1, p38, pp38, α-SMA and collagen Ⅰ were detected by immunohistochemistry, western blot and quantitative real-time PCR. The human hepatic stellate cell line LX2 was activated by TGF-β cytokine and the expression level of ARRB1 was analyzed. Furthermore, siRNA or plasmid was used to silence or overexpress ARRB1, and p38 specific inhibitor (SB203580) was adopted to reveal the regulatory relationship between ARRB1 and p38. Results ARRB1 expression was up-regulated and the activation of p38 signal was strengthened in liver fibrosis tissues(all P < 0.05). TGF-β treatment activated hepatic stellate cells and ARRB1 and p38 signaling in hepatic stellate cell LX2. The up-regulation or down-regulation of ARRB1 expression level could correspondingly affect p38 signaling and regulate the activity of hepatic stellate cells, while the change of p38 activity exerted no effect uponthe expression of ARRB1. Conclusion The expression level of ARRB1 is up-regulated in liver fibrosis, which can activate hepatic stellate cells by activating the p38 signaling, thereby promoting the incidence and development of liver fibrosis.https://www.xinyixue.cn/fileup/0253-9802/PDF/1676008145801-948190697.pdf|liver fibrosis|β-arrestin1|hepatic stellate cell|p38
spellingShingle Xia Yanhao, Liu Huiling, Jiang Jie, Wu Bin
β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway
Xin yixue
|liver fibrosis|β-arrestin1|hepatic stellate cell|p38
title β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway
title_full β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway
title_fullStr β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway
title_full_unstemmed β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway
title_short β-arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway
title_sort β arrestin1 activates hepatic stellate cells to promote liver fibrosis via activating p38 signaling pathway
topic |liver fibrosis|β-arrestin1|hepatic stellate cell|p38
url https://www.xinyixue.cn/fileup/0253-9802/PDF/1676008145801-948190697.pdf
work_keys_str_mv AT xiayanhaoliuhuilingjiangjiewubin barrestin1activateshepaticstellatecellstopromoteliverfibrosisviaactivatingp38signalingpathway