Cellular signalling · 2023
TRPV4 blockade alleviates endoplasmic reticulum stress mediated apoptosis in hypoxia-induced cardiomyocyte injury.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Li Xueqing, Lu Kongli, Guo Suxiang, Xue Song, Lian Feng
Аннотация
BACKGROUND: Hypoxia-induced myocardial injury remains to be a huge health issue worldwide. Transient receptor potential vanilloid 4 (TRPV4) is a high-flux Ca2+ channel that is involved in numerous cardiovascular diseases. However, the role of TRPV4 in myocardial hypoxic injury remains unclear. Accordingly, this study aimed to investigate the antiapoptotic activity of TRPV4 inhibition and elucidate the underlying mechanisms in myocardial hypoxic injury.
METHODS: The ability of TRPV4 to modulate the endoplasmic reticulum stress (ERS) and apoptosis was assessed in vitro through the administration of the TRPV4 antagonist HC-067047 or the agonist GSK1016790A. Additionally, intracellular Ca2+ concentration was measured by Fluo-4 AM.
RESULTS: TRPV4 expression was significantly upregulated in hypoxic H9c2 cells compared with that in normoxic cardiomyocytes, accompanied with increased intracellular Ca2+ levels. Conversely, TRPV4 inhibition alleviated ERS in hypoxic H9c2 cells and prevented apoptosis, whereas TRPV4 agonist exacerbated such events. Furthermore, H9c2 cell apoptosis was attenuated with the administration of 4-PBA, an ERS inhibitor.
CONCLUSION: TRPV4 inhibition alleviates hypoxia-induced H9c2 cell apoptosis by mitigating ERS.
METHODS: The ability of TRPV4 to modulate the endoplasmic reticulum stress (ERS) and apoptosis was assessed in vitro through the administration of the TRPV4 antagonist HC-067047 or the agonist GSK1016790A. Additionally, intracellular Ca2+ concentration was measured by Fluo-4 AM.
RESULTS: TRPV4 expression was significantly upregulated in hypoxic H9c2 cells compared with that in normoxic cardiomyocytes, accompanied with increased intracellular Ca2+ levels. Conversely, TRPV4 inhibition alleviated ERS in hypoxic H9c2 cells and prevented apoptosis, whereas TRPV4 agonist exacerbated such events. Furthermore, H9c2 cell apoptosis was attenuated with the administration of 4-PBA, an ERS inhibitor.
CONCLUSION: TRPV4 inhibition alleviates hypoxia-induced H9c2 cell apoptosis by mitigating ERS.