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"Mechanisms of Cardioprotection by Hsp22"

by
Paulo Lizano
MD/PhD Program
B.S. 2006, Rutgers University




Thesis Advisor: Christophe Depre, Ph.D., M.D.
Adjunct Associate Professor
Department of Cell Biology and Molecular Medicine

Friday, April 29, 2011
MSB G-606 Conference Room, 1:30 P.M.


Abstract

Expression of the molecular chaperone H11 kinase/Hsp22 (Hsp22) is restricted to the heart and skeletal muscle, both in rodents and in humans. In the heart, Hsp22 stimulates cardiac cell survival through a bone morphogenetic protein-mediated activation of the PI3K/Akt pathway that leads to the expression of the inducible nitric oxide (NO) synthase (iNOS) and subsequent cardioprotection against ischemic damage. The goal of the present study was to elucidate the downstream effector by which Hsp22 and Akt increase iNOS expression. In the first part, we hypothesized that the valosin-containing protein (VCP), an Akt substrate, which activates the transcription factor NF-B, plays a critical role in that process. In the second part, we investigate the role of the Signal Transducer and Activator of Transcription-3 (STAT3) in iNOS-dependent cardioprotective effects of Hsp22. Our results demonstrate that both VCP and STAT3 pathways mediate the increased expression of iNOS and the pro-survival effects downstream of Hsp22.


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