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Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p.
Wei, Peng; Dong, Zhifeng; Lou, Ming.
Afiliación
  • Wei P; Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China.
  • Dong Z; Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China.
  • Lou M; Department of Cardiology, Xuzhou Central Hospital, The Affiliated Xuzhou Hospital of Medical School of Southeast University, Xuzhou, Jiangsu, 221009, China.
Iran J Public Health ; 51(10): 2281-2288, 2022 Oct.
Article en En | MEDLINE | ID: mdl-36415802
ABSTRACT

Background:

LncRNA FGD5-AS1 regulates the pathogenesis of many human diseases. We aimed to elucidate the function of lncRNA FGD5-AS1 and the regulatory mechanism of lncRNA FGD5-AS1/miR-129-5p in myocardial ischemia-reperfusion (I/R) injury.

Methods:

Myocardial I/R injury mice model and H/R treated H9c2 cells were established. RT-qPCR and Western blot analysis were used to detect the mRNA and protein expression. Cell viability was detected by MTT assay. Dual luciferase reporter assay was applied to confirm the relationship between lncRNA FGD5-AS1 and miR-129-5p.

Results:

LncRNA FGD5-AS1 was upregulated in myocardial I/R injury mice models and H/R treated H9c2 cells. Functionally, knockdown of lncRNA FGD5-AS1 promoted cell viability and inhibited apoptosis in H/R treated H9c2 cells. In addition, lncRNA FGD5-AS1 directly targets miR-129-5p. Upregulation of lncRNA FGD5-AS1 weakened the protective effect of miR-129-5p on myocardial I/R injury.

Conclusion:

LncRNA FGD5-AS1 aggravates myocardial I/R injury by downregulating miR-129-5p.
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Iran J Public Health Año: 2022 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Iran J Public Health Año: 2022 Tipo del documento: Article País de afiliación: China
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