LncRNA GASL1 is downregulated in chronic heart failure and regulates cardiomyocyte apoptosis
Autor: | Li Zhang, Haihong Deng, Zhiyong Huang, Xiaoshan Xiao, Wendian Zhu, Wenbo Ouyang |
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Rok vydání: | 2019 |
Předmět: |
Adult
Male 0301 basic medicine lncRNA GASL1 Period (gene) Apoptosis Biochemistry Transforming Growth Factor beta1 Andrology 03 medical and health sciences 0302 clinical medicine Western blot TGF-β1 Research Letter medicine Humans Myocytes Cardiac Cancer biology lcsh:QH573-671 Molecular Biology Aged Heart Failure medicine.diagnostic_test lcsh:Cytology business.industry Cell Biology Plasma levels Middle Aged medicine.disease Molecular medicine Chronic heart failure 030104 developmental biology Gene Expression Regulation 030220 oncology & carcinogenesis Heart failure Chronic Disease Female RNA Long Noncoding business Cardiomyocyte apoptosis |
Zdroj: | Cellular & Molecular Biology Letters Cellular & Molecular Biology Letters, Vol 24, Iss 1, Pp 1-7 (2019) |
ISSN: | 1689-1392 1425-8153 |
DOI: | 10.1186/s11658-019-0165-x |
Popis: | Background TGF-β1 contributes to chronic heart failure. It is known that lncRNA GASL1 can inactivate TGF-β1 in cancer biology. Methods All the participants were enrolled in the First People’s Hospital of Zhaoqing during the period June 2012 to June 2013. ELISA, RT-qPCR, vectors, transient transfections and western blot were carried out during the research. Results We found that plasma levels of TGF-β1 were significantly higher, while levels of GASL1 in plasma were significantly lower in chronic heart failure (CHF) patients compared to the control group. TGF-β1 and GASL1 were inversely correlated in CHF patients. Low pretreatment plasma levels of GASL1 were closely associated with poor survival of CHF patients. GASL1 expression was not significantly affected by TGF-β1 overexpression in cardiomyocytes, while cardiomyocytes with GASL1 overexpression showed downregulated TGF-β1. Overexpression of GASL1 led to a decreased, while TGF-β1 overexpression led to an increased apoptotic rate of cardiomyocytes under H2O2 treatment. In addition, TGF-β1 overexpression attenuated the effect of GASL1 overexpression. Conclusion In conclusion, GASL1 was downregulated in CHF. GASL1 overexpression may improve CHF by inhibiting cardiomyocyte apoptosis through the inactivation of TGF-β1. |
Databáze: | OpenAIRE |
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