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LncRNA GASL1 is downregulated in chronic heart failure and regulates cardiomyocyte apoptosis
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 transfec...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6567419/ https://www.ncbi.nlm.nih.gov/pubmed/31223316 http://dx.doi.org/10.1186/s11658-019-0165-x |
Sumario: | 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 H(2)O(2) 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. |
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