Key result
Urotensin II pretreatment significantly reduced H2O2-induced apoptosis in cultured cardiomyocytes by increasing H2S production and CSE levels via ERK signaling activation.
Why the study?
Does urotensin II pretreatment prevent apoptosis in cultured cardiomyocytes exposed to oxidative stress?
Does urotensin II pretreatment prevent apoptosis in cultured cardiomyocytes exposed to oxidative stress?
Urotensin II protects cultured cardiomyocytes from oxidative stress-induced apoptosis via the CSE/H2S and ERK signaling pathways, suggesting a potential early protective role in acute myocardial infarction.
May attenuate oxidative cardiomyocyte injury in vitro; leaves open translation to in vivo infarction models.
Plasma urotensin II (UII) has been observed to be raised in patients with acute myocardial infarction; suggesting a possible cardiac protective role for this peptide. However, the molecular mechanism is unclear. Here, we treated cultured cardiomyocytes with H2O2 to induce oxidative stress; observed the effect of UII on H2O2-induced apoptosis and explored potential mechanisms. UII pretreatment significantly reduced the number of apoptotic cardiomyocytes induced by H2O2; and it partly abolished the increase of pro-apoptotic protein Bax and the decrease of anti-apoptotic protein Bcl-2 in cardiomyocytes induced by H2O2. SiRNA targeted to the urotensin II receptor (UT) greatly inhibited these effects. Further analysis revealed that UII increased the production of hydrogen sulfide (H2S) and the level of cystathionine-γ-lyase (CSE) by activating the ERK signaling in H2O2-treated-cardiomyocytes. Si-CSE or ERK inhibitor not only greatly inhibited the increase in CSE level or the phosphorylation of ERK induced by UII but also reversed anti-apoptosis of UII in H2O2-treated-cadiomyocytes. In conclusion, UII rapidly promoted the phosphorylation of ERK and upregulated CSE level and H2S production, which in turn activated ERK signaling to protect cardiomyocytes from apoptosis under oxidative stress. These results suggest that increased plasma UII level may protect cardiomyocytes at the early-phase of acute myocardial infarction in patients.
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Gong et al. (2015) studied Oxidative stress-induced apoptosis in cardiomyocytes. Urotensin II (UII) vs. H2O2 alone was evaluated on Apoptosis of cardiomyocytes. Urotensin II pretreatment significantly reduced H2O2-induced apoptosis in cultured cardiomyocytes by increasing H2S production and CSE levels via ERK signaling activation.
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