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Title:
Impairment of cardioprotective PI3K-Akt signaling by post-infarct ventricular remodeling is compensated by an ERK-mediated pathway | Basic Research in Cardiology
Description:
Recently we found that post-infarct remodeling disrupts PI3KAkt signaling triggered by erythropoietin (EPO) but an unknown compensatory mechanism preserves EPO-induced protection against infarction in those hearts. In this study, we examined the possibility that ERK-mediated signaling is the compensatory mechanism affording protection in post-infarct remodeled hearts. Four weeks after coronary ligation in situ (post-MI group, post-MI) or a sham operation (sham group, Sham), hearts were isolated, perfused and subjected to 25-min global ischemia/2-h reperfusion. Infarct size was expressed as a percentage of risk area size (%I/R), from which scarred infarct by coronary ligation was excluded. EPO infusion (5 U/ml) before ischemia reduced %I/R similarly in Sham and post-MI (from 62.0 ± 5.1 to 39.4 ± 4.8 in Sham and from 58.6 ± 6.6 to 36.3 ± 3.8 in post-MI). PD98059, a MEK1/2 inhibitor, abolished this EPO-induced protection in post-MI (%I/R = 60.7 ± 4.9) but not in Sham (%I/R = 35.1 ± 5.4). EPO induced PI3Kdependent phosphorylation of Akt in Sham but not in post-MI. EPO increased phosphorylation levels of ERK1/2 both in Sham and post-MI, but this phosphorylation was diminished by a PI3K inhibitor in Sham but not in post-MI. These results suggest that PI3K-independent activation of ERK compensates the lack of signal input from the PI3K-Akt pathway to achieve EPO-induced protection in the remodeled myocardium.
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article, google, scholar, cas, pubmed, signaling, miura, sham, miki, erythropoietin, postmi, activation, myocardial, kinase, basic, postinfarct, remodeling, pathway, tanno, shimamoto, protection, ventricular, hearts, erk, access, privacy, cookies, content, research, pikakt, infarction, phosphorylation, signal, res, preconditioning, publish, search, cardioprotective, nishihara, takahashi, epo, mechanism, remodeled, coronary, infarct, size, effect, ischemic, injury, cardiol,
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month download article/chapter glycogen synthase kinase-3β cardioprotective pi3k-akt signaling post-infarct remodeled hearts post-infarct ventricular remodeling erythropoietin-induced cardioprotective signaling achieve epo-induced protection erythropoietin-mediated acute protection article basic research myocardial infarct size pi3k-akt pathway erk-mediated signaling p44/p42 mapks phosphatidylinositol- 3-kinase signaling phosphatidylinositol 3-kinase signaling epo-induced protection postinfarct remodeled hearts postinfarct ventricular remodeling full article pdf myocardial ischemia/reperfusion injury privacy choices/manage cookies erk-mediated pathway risk area size pi3k-independent activation erythropoietin-mediated cardioprotection acute myocardial infarction primary erythroid progenitors infarct size factorial randomized trial primes gsk-3β signal transduction mediated remote ischemic conditioning pkc-dependent activation prior myocardial infarction ventricular remodeling european economic area scope submit manuscript prodromal angina pectoris pkc-ε underlies van de werf protein kinase ischaemic preconditioning effect conditions privacy policy myocardial ischemia-reperfusion turning cells red 25-min global ischemia/2 article miki impaired myocardial response ischemia- reperfusion injury accepting optional cookies
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headline:Impairment of cardioprotective PI3K-Akt signaling by post-infarct ventricular remodeling is compensated by an ERK-mediated pathway
description:Recently we found that post-infarct remodeling disrupts PI3KAkt
signaling triggered by erythropoietin (EPO) but an unknown compensatory
mechanism preserves EPO-induced protection against infarction in
those hearts. In this study, we examined the possibility that ERK-mediated
signaling is the compensatory mechanism affording protection in post-infarct
remodeled hearts. Four weeks after coronary ligation in situ (post-MI
group, post-MI) or a sham operation (sham group, Sham), hearts were isolated,
perfused and subjected to 25-min global ischemia/2-h reperfusion. Infarct
size was expressed as a percentage of risk area size (%I/R), from which
scarred infarct by coronary ligation was excluded. EPO infusion (5 U/ml) before
ischemia reduced %I/R similarly in Sham and post-MI (from 62.0 ± 5.1
to 39.4 ± 4.8 in Sham and from 58.6 ± 6.6 to 36.3 ± 3.8 in post-MI). PD98059,
a MEK1/2 inhibitor, abolished this EPO-induced protection in post-MI
(%I/R = 60.7 ± 4.9) but not in Sham (%I/R = 35.1 ± 5.4). EPO induced PI3Kdependent
phosphorylation of Akt in Sham but not in post-MI. EPO increased
phosphorylation levels of ERK1/2 both in Sham and post-MI, but
this phosphorylation was diminished by a PI3K inhibitor in Sham but not in
post-MI. These results suggest that PI3K-independent activation of ERK
compensates the lack of signal input from the PI3K-Akt pathway to achieve
EPO-induced protection in the remodeled myocardium.
datePublished:2006-09-01T00:00:00Z
dateModified:2006-09-01T00:00:00Z
pageStart:163
pageEnd:170
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ERK
remodeled hearts
infarct
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headline:Impairment of cardioprotective PI3K-Akt signaling by post-infarct ventricular remodeling is compensated by an ERK-mediated pathway
description:Recently we found that post-infarct remodeling disrupts PI3KAkt
signaling triggered by erythropoietin (EPO) but an unknown compensatory
mechanism preserves EPO-induced protection against infarction in
those hearts. In this study, we examined the possibility that ERK-mediated
signaling is the compensatory mechanism affording protection in post-infarct
remodeled hearts. Four weeks after coronary ligation in situ (post-MI
group, post-MI) or a sham operation (sham group, Sham), hearts were isolated,
perfused and subjected to 25-min global ischemia/2-h reperfusion. Infarct
size was expressed as a percentage of risk area size (%I/R), from which
scarred infarct by coronary ligation was excluded. EPO infusion (5 U/ml) before
ischemia reduced %I/R similarly in Sham and post-MI (from 62.0 ± 5.1
to 39.4 ± 4.8 in Sham and from 58.6 ± 6.6 to 36.3 ± 3.8 in post-MI). PD98059,
a MEK1/2 inhibitor, abolished this EPO-induced protection in post-MI
(%I/R = 60.7 ± 4.9) but not in Sham (%I/R = 35.1 ± 5.4). EPO induced PI3Kdependent
phosphorylation of Akt in Sham but not in post-MI. EPO increased
phosphorylation levels of ERK1/2 both in Sham and post-MI, but
this phosphorylation was diminished by a PI3K inhibitor in Sham but not in
post-MI. These results suggest that PI3K-independent activation of ERK
compensates the lack of signal input from the PI3K-Akt pathway to achieve
EPO-induced protection in the remodeled myocardium.
datePublished:2006-09-01T00:00:00Z
dateModified:2006-09-01T00:00:00Z
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