AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 288: H3006-H3010, 2005. First published January 21, 2005; doi:10.1152/ajpheart.01203.2004
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Potential candidates for ischemic preconditioning-associated vascular growth pathways revealed by antibody array

Praveer Mathur, Shigeaki Kaga, Lijun Zhan, Dipak K. Das, and Nilanjana Maulik

Molecular Cardiology Laboratory, Department of Surgery, University of Connecticut Health Center, Farmington, Connecticut

Submitted 1 December 2004 ; accepted in final form 17 January 2005

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 four in vivo repetitive cycles of coronary artery occlusion, each followed by reperfusion as the model to stimulate vascular growth, and performed the protein profiling using high-throughput antibody array technology. Rats were divided into two 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, granulocyte-monocyte colony-stimulating factor, signal transducer and activator of transcription 3, {alpha}- and {beta}-catenins, ubiquitin-conjugating enzyme UbcH6, nexilin, and PKC-{epsilon} and -{lambda}. JNK1 and 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 valid participants in the vascular growth signals that are known to be triggered by ischemic preconditioning of heart.

myocardial infarction; signal transduction



Address for reprint requests and other correspondence: N. Maulik, Molecular Cardiology Laboratory, Dept. of Surgery, Univ. of Connecticut School of Medicine, Farmington, CT 06030-1110 (E-mail: nmaulik{at}neuron.uchc.edu)




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