Restoration of YAP activation rescues HL-1 cardiomyocytes from apoptotic death by ethanol

Abstract

-We reported previously that when mouse atrium-derived HL-1 cardiomyocytes undergo apoptosis upon exposure to 2% ethanol, the cellular cytoskeleton is severely disrupted and the anti-apoptotic transcriptional co-activator Yes-associated protein (YAP) is inactivated. Consistent with our previous observations, the expression of connective tissue growth factor (CTGF), an anti-apoptotic growth factor and a target of YAP, decreases in a time-dependent manner during exposure to 2% ethanol. The restoration of YAP activation rescues the cells from apoptosis: both the retrovirus-mediated expression of constitutively active YAP and the stabilization of the actomyosin cytoskeleton by jasplakinolide prevent cell death. In contrast, YAP inhibitors have no effect on cell death, confirming the inactivation of YAP in ethanol-exposed cells. Thus, a decrease in actin tension and YAP inactivation should be crucially involved in the cytotoxicity of ethanol on HL-1 cardiomyocytes.

Pyroptotic cell death by exposure to 1-butanol in H9c2 cardiomyoblastoma cells

“…2.3. Quantitative real time reverse-transcriptase-mediated PCR (qPCR) qPCR was performed as described previously (Noritake et al, 2015;Noritake et al, 2017). In brief, total RNA was extracted from the cells using Trizol reagent (Thermo Fisher Scientific) and reverse-transcription was performed using SuperScript II (Thermo Fisher Scientific).…”