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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 7410257, 14 pages
http://dx.doi.org/10.1155/2016/7410257
Research Article

CD38 Deficiency Protects the Heart from Ischemia/Reperfusion Injury through Activating SIRT1/FOXOs-Mediated Antioxidative Stress Pathway

1Institute of Translational Medicine, Nanchang University, Nanchang 330031, China
2National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China
3Department of Basic Medical Science, Shock/Trauma Research Center, School of Medicine, University of Missouri-Kansas City, Kansas City, MO 64108, USA

Received 7 April 2016; Revised 25 May 2016; Accepted 14 June 2016

Academic Editor: Massimo Collino

Copyright © 2016 Xiao-Hui Guan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Figure S1. The effects of sham operation on hearts. The Sham-operated animals were subjected to the same surgical procedures, except that the suture was passed under the LAD but not tied. The hearts from wild type and CD38 KO mice with sham operation were stained with evens blue/TTC staining and there was no infarct area in these groups (n = 5). Figure S2. The mRNA expressions of CD38 in H9c2 cells. The mRNA expressions of CD38 were determined by qPCR when a CD38 expression vector was introduced into the normal and CD38 knockdown H9c2 cells. ***p<0.001, n = 3. Figure S3. Effects of CD38 overexpression on cell viabilities after H/R stimulation. Cell viability was analyzed by CCK8 assay with various cells after CD38 expression vector was introduced into the cells followed with H/R stimulation. After H/R stimulation, the viabilities of CD38 knockdown H9c2 cells were significantly increased compared with the control cells, whereas the increased CD38 expressions of the normal or CD38 knockdown cells by introducing CD38 expression vector markedly attenuated the cell viabilities. *p<0.05, **p<0.01, ***p<0.001, n=5. Figure S4. Effects of CD38 overexpression on apoptosis in H9c2 cells. The H/R induced apoptosis of H9c2 cells were examined by annexinV/PI staining assay after transfected with the CD38 expression vector. The apoptosis in CD38 overexpressing cells was significantly increased compared with normal H9c2 cells after H/R stimulation. ***p<0.001, n = 3.

  1. Supplementary Material