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Protective effects of kenpaullone on cardiomyocytes following H2O2-induced oxidative stress are attributed to inhibition of connexin 43 degradation by SGSM3.

Abstract：

:A previous study showed that small G protein signaling modulator 3 (SGSM3) was highly correlated with Cx43 in heart functions and that high levels of SGSM3 may induce Cx43 turnover through lysosomal degradation in infarcted rat hearts. Here, we investigated the protective effects of kenpaullone on cardiomyocytes following H2O2-induced oxidative stress mediated by the interaction of SGSM3 with Cx43. We found that the gap junction protein Cx43 was significantly down-regulated in an H2O2 concentration-dependent manner, whereas expression of SGSM3 was up-regulated upon H2O2 exposure in H9c2 cells. The effect of kenpaullone pretreatment on H2O2-induced cytotoxicity was evaluated in H9c2 cells. H2O2 markedly increased the release of lactate dehydrogenase (LDH), while kenpaullone pretreatment suppressed LDH release in H9c2 cells. Moreover, kenpaullone pretreatment significantly reduced ROS fluorescence intensity and significantly down-regulated the level of apoptosis-activating genes (cleaved caspase-3, cleaved caspase-9 and cytochrome C), autophagy markers (LC3A/B), and the Cx43-interacting partner SGSM3. These results suggest that kenpaullone plays a role in protecting cardiomyocytes from oxidative stress and that the turnover of Cx43 through SGSM3-induced lysosomal degradation underlies the anti-apoptotic effect of kenpaullone.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Joo HC,Choi JW,Moon H,Lee CY,Yoo KJ,Kim SW,Hwang KC

doi

10.1016/j.bbrc.2018.03.166

subject

Has Abstract

pub_date

2018-05-05 00:00:00

pages

368-373

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)30684-3

journal_volume

499

pub_type

杂志文章

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