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Activated protein C prevents methylglyoxal-induced endoplasmic reticulum stress and cardiomyocyte apoptosis via regulation of the AMP-activated protein kinase signaling pathway

Title
Activated protein C prevents methylglyoxal-induced endoplasmic reticulum stress and cardiomyocyte apoptosis via regulation of the AMP-activated protein kinase signaling pathway
Authors
Nam D.-H.Han J.-H.Kim S.Shin Y.Lim J.H.Choi H.C.Woo C.-H.
Ewha Authors
임재향
SCOPUS Author ID
임재향scopus
Issue Date
2016
Journal Title
Biochemical and Biophysical Research Communications
ISSN
0006-291XJCR Link
Citation
vol. 480, no. 4, pp. 622 - 628
Keywords
AMPKAPCCardiomyocyteCHOPER stressMethylglyoxal
Publisher
Elsevier B.V.
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Previous epidemiological studies have shown that methylglyoxal (MGO) levels are highly regulated in diabetic cardiovascular diseases. We have also previously reported that MGO mediates ER stress and apoptosis in cardiomyocytes. Furthermore, activated protein C (APC) has recently been shown to play a protective role against ER stress, as well as a cardioprotective role against ischemia and reperfusion injury by augmenting the AMP-activated protein kinase (AMPK) signaling pathway. Therefore, we hypothesized that APC protects against MGO-induced cardiomyocyte apoptosis through the inhibition of ER stress. Our results showed that APC inhibited MGO-induced cardiomyocyte apoptosis and ER stress-related gene expression. Additionally, APC inhibited MGO-induced Ca2+ mobilization and the generation of reactive oxygen species. In contrast, inhibitors of AMPK signaling abolished the cytoprotective effects of APC. Collectively, these data depict a pivotal role for AMPK signaling in inhibiting ER stress responses via the activation of APC during MGO-induced cardiomyocyte apoptosis. Thus, APC may be a potential novel therapeutic target for the management of diabetic cardiovascular complications such as diabetic cardiomyopathy. © 2016 Elsevier Inc.
DOI
10.1016/j.bbrc.2016.10.106
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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