Abstract:
:Glycogen synthase kinase (GSK)-3β interaction protein (GSKIP), a key regulator of signaling transduction, is implicated in multiple pathological processes. However, whether GSKIP is involved in myocardial infarction is unknown. The present study was designed to determine the potential involvement of GSKIP in myocardial hypoxia/reoxygenation (H/R) injury, as an in vitro model for the study of myocardial infarction. Our data showed that H/R treatment triggered a marked decrease in GSKIP expression in cardiomyocytes. The upregulation of GSKIP significantly rescued the decreased viability of H/R-exposed cardiomyocytes and attenuated H/R-induced apoptosis and reactive oxygen species (ROS) generation. On the contrary, the depletion of GSKIP enhanced the sensitivity of cardiomyocytes to H/R-induced injury. Further data exhibited that GSKIP overexpression upregulated the nuclear expression of nuclear factor-erythroid-derived 2-related factor 2 (Nrf2) and increased Nrf2/antioxidant response element (ARE)-mediated transcription activity associated with upregulation of GSK-3β phosphorylation. Interestingly, inhibition of GSK-3β by a chemical inhibitor markedly enhanced Nrf2/ARE activation and abrogated GSKIP depletion-exacerbated sensitivity to H/R-induced injury. In addition, Nrf2 inhibition markedly reversed GSKIP overexpression-induced cardioprotective effect against H/R injury. Overall, these results demonstrate that overexpression of GSKIP alleviates H/R-induced apoptosis and oxidative stress in cardiomyocytes by enhancing Nrf2/ARE antioxidant signaling via GSK-3β inhibition. Our study indicates a potential role of GSKIP in myocardial infarction and GSKIP may serve as a promising molecular target for cardioprotection.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Yan L,Cheng G,Yang Gdoi
10.1016/j.bbrc.2020.06.029subject
Has Abstractpub_date
2020-10-29 00:00:00pages
68-75issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(20)31230-4journal_volume
532pub_type
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
doi:10.1016/0006-291x(86)90409-2
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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更新日期:2009-07-31 00:00:00
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更新日期:1984-06-29 00:00:00
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更新日期:2014-06-13 00:00:00
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
doi:10.1006/bbrc.2002.6628
更新日期:2002-03-22 00:00:00
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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journal_title:Biochemical and biophysical research communications
pub_type: 杂志文章
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更新日期:1983-01-14 00:00:00