原创力文档camkiiδb mediates aberrant ncx1 expression and the imbalance of ncx1serca in transverse aortic constriction-induced failing heartcamkiiδb调节异常ncx1表达和ncx1serca失衡的横向主动脉constriction-induced失败的心.pdfVIP
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camkiiδb mediates aberrant ncx1 expression and the imbalance of ncx1serca in transverse aortic constriction-induced failing heartcamkiiδb调节异常ncx1表达和ncx1serca失衡的横向主动脉constriction-induced失败的心
CaMKIIdB Mediates Aberrant NCX1 Expression and the
Imbalance of NCX1/SERCA in Transverse Aortic
Constriction-Induced Failing Heart
2,3 1 3 3 4 2
Ying-Mei Lu , Jiyun Huang , Norifumi Shioda , Kohji Fukunaga , Yasufumi Shirasaki , Xiao-ming Li ,
Feng Han1*
1 Institute of Pharmacology, Toxicology and Biochemical Pharmaceutics, Zhejiang University, Hangzhou, China, 2 Department of Neurobiology, Zhejiang University School
of Medicine, Hangzhou, China, 3 Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan, 4 Biological Research
Laboratories, Daiichi-Sankyo Pharmaceutical Co., Ltd. Tokyo, Japan
Abstract
Ca2+/calmodulin-dependent protein kinase II dB (CaMKIIdB) is one of the predominant isoforms of CaMKII in the heart. The
precise role of CaMKIIdB in the transcriptional cross-talk of Ca2+-handling proteins during heart failure remains unclear. In
+ 2+
this work, we aim to determine the mechanism of CaMKIIdB in modulating the expression of sarcolemmal Na –Ca
exchange (NCX1). We also aim to address the potential effects of calmodulin antagonism on the imbalance of NCX1 and
sarcoendoplasmic reticulum Ca2+ ATPase (SERCA) during heart failure. Eight weeks after transverse aortic constriction (TAC)-
induced heart failure in mice, we found that the heart weight/tibia length (HW/TL) ratio and the lung weight/body weight
(LW/BW) ratio increased by 59% and 133%, respectively. We further found that the left ventricle-shortening fraction
decreased by 40% compared with the sham-operated controls. Immunoblott
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