ca+2calmodulin-dependent protein kinase mediates glucose toxicity-induced cardiomyocyte contractile dysfunctionca + 2 calmodulin-dependent蛋白激酶介导葡萄糖toxicity-induced心肌细胞收缩功能障碍.pdfVIP

Hindawi Publishing Corporation Experimental Diabetes Research Volume 2012, Article ID 829758, 11 pages doi:10.1155/2012/829758 Research Article Ca+2/Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction Rong-Huai Zhang,1 Haitao Guo,2 Machender R. Kandadi,3 Xiao-Ming Wang,1 and Jun Ren1, 2, 3 1 Department of Geriatrics, Xijing Hospital, The Fourth Military Medical University, Xi’an 710032, China 2 Department of Physiology, The Fourth Military Medical University, Xi’an 710032, China 3 Division of Pharmaceutical Sciences, University of Wyoming, College of Health Sciences, Laramie, WY 82071, USA Correspondence should be addressed to Xiao-Ming Wang, xmwang@fmmu.edu.cn and Jun Ren, jren@uwyo.edu Received 22 March 2012; Accepted 29 March 2012 Academic Editor: Yingmei Zhang Copyright © 2012 Rong-Huai Zhang 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. (1) Hyperglycemia leads to cytotoxicity in the heart. Although several theories are postulated for glucose toxicity-induced cardiomyocyte dysfunction, the precise mechanism still remains unclear. (2) This study was designed to evaluate the impact of elevated extracellular Ca2+ on glucose toxicity-induced cardiac contractile and intracellular Ca2+ anomalies as well as the mechanism(s) involved with a focus on Ca2+/calmodulin (CaM)-dependent kinase. Isolated adult rat cardiomyocytes were maintained in normal (NG, 5.5 mM) or high glucose (HG, 25.5 mM) media for 6-12 hours. Contractile indices were measured including peak shortening (PS), maximal velo