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MALAT1-mediated EZH2 Recruitment to the GFER Promoter Region Curbs Normal Hepatocyte Proliferation in Acute Liver Injury.
Chen, Li; Kang, Xintong; Meng, Xiujuan; Huang, Liang; Du, Yiting; Zeng, Yilan; Liao, Chunfeng.
Afiliación
  • Chen L; Department of Infectious Diseases, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
  • Kang X; Department of Hepatology, Public Health Clinical Center of Chengdu, Chengdu, Sichuan, China.
  • Meng X; Hospital-Acquired Infection Control Center, Xiangya Hospital Central South University, Changsha, Hunan, China.
  • Huang L; Department of Hepatology, Public Health Clinical Center of Chengdu, Chengdu, Sichuan, China.
  • Du Y; Department of Emergency, Chengdu Women's and Children's Central Hospital, Chengdu, Sichuan, China.
  • Zeng Y; Department of Hepatology, Public Health Clinical Center of Chengdu, Chengdu, Sichuan, China.
  • Liao C; Department of Cardiovascular Medicine, The First Hospital of Changsha, Changsha, Hunan, China.
J Clin Transl Hepatol ; 11(1): 97-109, 2023 Feb 28.
Article en En | MEDLINE | ID: mdl-36406327
Background and Aims: The goal of this study was to investigate the mechanism by which the long noncoding RNA MALAT1 inhibited hepatocyte proliferation in acute liver injury (ALI). Methods: Lipopolysaccharide (LPS) was used to induce an ALI cellular model in HL7702 cells, in which lentivirus vectors containing MALAT1/EZH2/GFER overexpression or knockdown were introduced. A series of experiments were performed to determine their roles in liver injury, oxidative stress injury, and cell biological processes. The interaction of MALAT1 with EZH2 and enrichment of EZH2 and H3K27me3 in the GFER promoter region were identified. Rats were treated with MALAT1 knockdown or GFER overexpression before LPS induction to verify the results derived from the in vitro assay. Results: MALAT1 levels were elevated and GFER levels were reduced in ALI patients and the LPS-induced cell model. MALAT1 knockdown or GFER overexpression suppressed cell apoptosis and oxidative stress injury induced cell proliferation, and reduced ALI. Functionally, MALAT1 interacted directly with EZH2 and increased the enrichment of EZH2 and H3K27me3 in the GFER promoter region to reduce GFER expression. Moreover, MALAT1/EZH2/GFER was activated the AMPK/mTOR signaling pathway. Conclusion: Our study highlighted the inhibitory role of reduced MALAT1 in ALI through the modulation of EZH2-mediated GFER.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Clin Transl Hepatol Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Clin Transl Hepatol Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos