Lack of Mof reduces acute liver injury by enhancing transcriptional activation of Igf1
Autor: | Wenbo Zhao, Xiangzhi Li, Chengpeng Xu, Danyang Li, Fei Xie, Haoyu Liu, Meng Wang, Xu Zhang, Zhen Wu |
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Rok vydání: | 2021 |
Předmět: |
Transcriptional Activation
0301 basic medicine Physiology animal diseases medicine.medical_treatment Clinical Biochemistry Adenoviridae 03 medical and health sciences Liver disease 0302 clinical medicine Cell Line Tumor medicine Animals Insulin-Like Growth Factor I Promoter Regions Genetic Carbon Tetrachloride Histone Acetyltransferases Liver injury Gene knockdown Chemistry Liver cell Growth factor fungi Imidazoles Cell Biology respiratory system medicine.disease Hepatic stellate cell activation Liver regeneration Liver Regeneration respiratory tract diseases Mice Inbred C57BL 030104 developmental biology Liver Gene Knockdown Techniques Pyrazines 030220 oncology & carcinogenesis Acute Disease Cancer research Signal transduction Protein Binding Signal Transduction |
Zdroj: | Journal of Cellular Physiology. 236:6559-6570 |
ISSN: | 1097-4652 0021-9541 |
DOI: | 10.1002/jcp.30332 |
Popis: | Acute liver injury (ALI) is a rapid pathological process that may cause severe liver disease and may even be life-threatening. During ALI, the function of males absent on the first (MOF) has not yet been elucidated. In this study, we unveiled the expression pattern of MOF during carbon tetrachloride (CCl4 )-induced ALI and role of MOF in the regulation of liver regeneration. In the process of ALI, MOF is significantly overexpressed in the liver injury area. Knockdown of Mof attenuated CCl4 -induced ALI, and promoted liver cell proliferation, hepatic stellate cell activation and aggregation to the injured area, and liver fibrosis. Simultaneously, overexpression of Mof aggravated liver dysfunction caused by ALI. By directly binding to the promoter, MOF suppressed the transcriptional activation of Igf1. Knockdown of Mof promotes the expression of Igf1 and activates the Insulin-like growth factor 1 signaling pathway in the liver. Through this pathway, Knockdown of Mof reduces CCl4 -induced ALI and promotes liver regeneration. Our results provide the first demonstration for MOF contributing to ALI. Further understanding of the role of MOF in ALI may lead to new therapeutic strategies for ALI. |
Databáze: | OpenAIRE |
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