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  • Title: [Effects of hydrogen sulfide (H2S) on cardiac hypertrophy and miRNA-133a-mediated Ca2+/calcineurin/NFATc4 signal pathway in rats].
    Author: Wu Y, Guo YY, Zhang YY, Zhang Y.
    Journal: Zhongguo Ying Yong Sheng Li Xue Za Zhi; 2018 Jan 08; 34(1):29-34. PubMed ID: 29926655.
    Abstract:
    OBJECTIVE: To investigate the effects of hydrogen sulfide (H2S) on the negatively regulation of cardiomyocyte hypertrophy and the relationship between the effect of H2S with miRNA-133a-mediated Ca2+/calcineurin/NFATc4 signal pathway. METHODS: Cardiomyocyte hypertrophy was induced by isoproterenol (ISO). The cell surface area was measured by image analysis system (Leica). The expression of brain natriuretic peptide(BNP), β-myosin heavy chain(β-MHC), cystathionase (CSE), miRNA-133a, calcineurin (CaN) were detected by qRT-PCR. The protein expressions of CaN、nuclear factors of activated T cells (NFATc4) were detected by Western blot. The concentration of H2S in the cardiomyocyte was detected by Elisa. The concentration of intracellular calcium was measured by calcium imaging using confocal microscope. The nuclear translocation of NFATc4 was checked by immuno-fluorescence cell staining technique. RESULTS: ①The level of system of CSE/H2S and expression of miRNA-133a were significantly reduced in cardiomyocyte hypertrophy. Pretreatment with NaHS increased the concentration of H2S and the expression of miRNA-133a mRNA in cardiomyocytes, and suppressed cardiomyocyte hypertrophy. ②The concentration of intracellular calcium, the expression of CaN and nulear protein NFATc4 were significantly increased, and the nuclear translocation of NFATc4 were obviously enhanced in cardiomyocyte hypertrophy. NaHS pretreatment markedly inhibited these effects of ISO induced cardiomyocyte hypertrophy. ③Application of antagomir-133a reversed the inhibitory effects of NaHS on cardiomyocyte hypertrophy, and increased the influx of intracellular calcium, and elevated the expression of CaN and nuclear protein NFATc4, and enhanced the nuclear translocation of NFATc4. CONCLUSIONS: H2S can negatively regulate cardiomyocyte hypertrophy. The effects might be associated with H2S increasing expression of miRNA-133a and inhibiting inactivation of Ca2+/calcineurin/NFATc4 signal pathway.
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