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1.
Biochem Biophys Res Commun ; 503(3): 1186-1193, 2018 09 10.
Article in English | MEDLINE | ID: mdl-30031611

ABSTRACT

This study aimed to investigate whether recombinant human brain natriuretic peptide (rhBNP) regulated hypoxia-induced injury in H9c2 cardiomyocytes through lncRNA EGOT. H9c2 cardiomyocytes were cultured under normoxia and hypoxia (21% and 3% O2) conditions, and whether hypoxia induced injury by assessing cell viability, apoptosis and autophagy. H9c2 cells were then treated with different doses of exogenous rhBNP (200, 600 and 900 nmol/L, respectively) and the effects of rhBNP on hypoxia-induced injury in H9c2 cells as well as the expression of EGOT were studied. In addition, the regulatory relationships between rhBNP and EGOT as well as between rhBNP and PI3K/AKT/mTOR pathway in hypoxia-treated H9c2 cells were investigated. Hypoxia significantly induced injury in H9c2 cells (inhibited cell viability and promoted cell apoptosis and autophagy) and decreased the expression of EGOT. However, administration of rhBNP alleviated hypoxia-induced injury in H9c2 cells and elevated expression of EGOT. Suppression of EGOT significantly reversed the effects of rhBNP on hypoxia-induced injury in H9c2 cells. Further studies showed that the effects of EGOT on cell viability and apoptosis were by positively regulating the expression of Cyclin D1. Moreover, rhBNP alleviated hypoxia-induced cell injury by activating PI3K/AKT/mTOR pathway in H9c2 cells. Our results reveal that rhBNP may play a protective role in attenuating hypoxia-induced injury in H9c2 cardiomyocytes via regulating lncRNA EGOT/Cyclin D1/PI3K/AKT/mTOR pathway axis. The findings will provide a new strategy for the treatment of heart failure induced by hypoxia.


Subject(s)
Myocytes, Cardiac/metabolism , Natriuretic Peptide, Brain/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , RNA, Long Noncoding/metabolism , TOR Serine-Threonine Kinases/metabolism , Apoptosis , Cells, Cultured , Humans , Hypoxia , Myocytes, Cardiac/pathology , Recombinant Proteins/metabolism
2.
Int J Clin Exp Pathol ; 11(9): 4512-4520, 2018.
Article in English | MEDLINE | ID: mdl-31949848

ABSTRACT

This study aimed to investigate the effects and mechanisms of long noncoding RNA SRA1 on regulating hypoxia-induced injury in H9c2 cardiomyocytes. The H9c2 cardiomyocytes were cultured under hypoxic (3% O2) conditions and whether hypoxia induced injury was assessed by detecting cell viability, apoptosis and autophagy. Then, SRA1 was overexpressed and suppressed in H9c2 cardiomyocytes by transfection with pc-SRA1 and sh-SRA1, and the effects of SRA1 dysregulation on cell viability, apoptosis, and autophagy of H9c2 cardiomyocytes under hypoxia condition were detected. Furthermore, the regulatory relationship between SRA1 and PPARγ was explored, as well as the association between SRA1 and NF-κB signaling. Hypoxia induced injury to H9c2 cardiomyocytes, such as inhibiting cell viability, and promoting cell apoptosis and autophagy. Moreover, hypoxia resulted in a decreased expression of SRA1 in H9c2 cardiomyocytes, and overexpression of SRA1 alleviated hypoxia-induced injury, while suppression of SRA1 indicated the contrary results. Further studies showed that SRA1 positively regulated PPARγ. Overexpression of SRA1 alleviated hypoxia injury by activating PPARγ. Besides, suppression of SRA1 activated NF-κB pathway in hypoxia-treated H9c2 cardiomyocytes, which were significantly reversed after suppression of SRA1 and overexpression of PPARγ at the same time. Our findings indicated that suppression of SRA1 may aggravate hypoxia-induced injury to H9c2 cardiomyocytes by positive regulation of PPARγ and activation of NF-κB pathway. SRA1 may serve as a promising perspective for the therapy of heart failure induced by hypoxia.

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