AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol (January 21, 2005). doi:10.1152/ajpheart.01203.2004
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Submitted on December 2, 2004
Accepted on January 17, 2005

Potential candidates for Ischemic Preconditioning associated vascular growth pathways revealed by Antibody Array

Praveer Mathur1, Shigeaki Kaga1, Lijun Zhan1, Dipak K Das1, and Nilanjana Maulik1*

1 Surgery, University of Connecticut Medical Center, Farmington, Connecticut, USA

* To whom correspondence should be addressed. E-mail: nmaulik{at}neuron.uchc.edu.

Our understanding of the phenomenon of myocardial vascular growth is very limited even though various studies have been conducted in several different models because the focus in each has been on a select very few number of proteins as the possible growth factors. In the present study, we used the ischemic preconditioning (IP) model in the form of in vivo four repetitive cycles of coronary artery occlusion each followed by reperfusion as the model to stimulate vascular growth and performed the protein profiling using the high throughput antibody array technology. Rats were divided into 2 groups: Control + Left anterior descending coronary artery (LAD) occlusion (CMI), and IP+ LAD occlusion (IPMI). The antibody array experiment performed to compare the expression of 512 proteins between the IPMI and CMI samples revealed significant upregulation of growth proteins like TGF {beta}, BMX, GM-CSF, Stat3, {alpha} and {beta} Catenins, UbcH6, Nexilin, and PKC {epsilon} and {lambda}. JNK1 and CSK(c-src tyrosine kinase) were expectedly found to be downregulated. Western blot experiments validated the changes in expression of these proteins. Therefore, this study puts forward the above mentioned proteins as the valid participants in the vascular growth signals that are known to be triggered by ischemic preconditioning of heart.







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