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Int. J. Mol. Sci. 2016, 17(4), 542; doi:10.3390/ijms17040542

Deficiency of Senescence Marker Protein 30 Exacerbates Cardiac Injury after Ischemia/Reperfusion

1
Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, 2-2-2 iidanihi, Yamagata 990-9585, Japan
2
Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo 173-0015, Japan
3
Department of Cardiology and Hematology, Fukushima Medical University, 1 Hikarigaoka, Fukushima 960-1295, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: Michael Henein
Received: 24 February 2016 / Revised: 1 April 2016 / Accepted: 2 April 2016 / Published: 11 April 2016
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
View Full-Text   |   Download PDF [3082 KB, uploaded 11 April 2016]   |  

Abstract

Early myocardial reperfusion is an effective therapy but ischemia/reperfusion (I/R) causes lethal myocardial injury. The aging heart was reported to show greater cardiac damage after I/R injury than that observed in young hearts. Senescence marker protein 30 (SMP30), whose expression decreases with age, plays a role in reducing oxidative stress and apoptosis. However, the impact of SMP30 on myocardial I/R injury remains to be determined. In this study, the left anterior descending coronary artery was occluded for 30 min, followed by reperfusion in wild-type (WT) and SMP30 knockout (KO) mice. After I/R, cardiomyocyte apoptosis and the ratio of infarct area/area at risk were higher, left ventricular fractional shortening was lower, and reactive oxygen species (ROS) generation was enhanced in SMP30 KO mice. Moreover, the previously increased phosphorylation of GSK-3β and Akt was lower in SMP30 KO mice than in WT mice. In cardiomyocytes, silencing of SMP30 expression attenuated Akt and GSK-3β phosphorylation, and increased Bax to Bcl-2 ratio and cardiomyocyte apoptosis induced by hydrogen peroxide. These results suggested that SMP30 deficiency augments myocardial I/R injury through ROS generation and attenuation of Akt activation. View Full-Text
Keywords: ischemia reperfusion; SMP30; cardiomyocyte; GSK-3β ischemia reperfusion; SMP30; cardiomyocyte; GSK-3β
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Kadowaki, S.; Shishido, T.; Sasaki, T.; Sugai, T.; Narumi, T.; Honda, Y.; Otaki, Y.; Kinoshita, D.; Takahashi, T.; Nishiyama, S.; Takahashi, H.; Arimoto, T.; Miyamoto, T.; Watanabe, T.; Ishigami, A.; Takeishi, Y.; Kubota, I. Deficiency of Senescence Marker Protein 30 Exacerbates Cardiac Injury after Ischemia/Reperfusion. Int. J. Mol. Sci. 2016, 17, 542.

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