Grant: $369,050 - National Institutes of Health - Sep. 28, 2009
No votes have been cast for this award yet
Award Description: We propose that the recruitment of endothelial progenitor cells and activation of anti-inflammatory signaling pathways are the mechanisms by which SDF-1? is beneficial in sepsis. 1. We will determine the effect of CTCE-0214 on the cecal ligation and puncture (CLP)-induced recruitment of endothelial progenitor cells (EPC)s and inflammatory response. CD-1 mice will be subjected to CLP followed by injection of CTCE-0214. EPCs levels and CLP-induced inflammation will be studied. 2. We will investigate the mechanism by which SDF-1? and CTCE-0214 recruit EPCs and suppress the inflammatory response. EPCs, BMDM, mouse aortic endothelial cell (MAEC) and splenic CD4+ T cells will be isolated from wild type and the novel G?i2 knockout and G?i2 gain of function mice. Induction of chemotaxis of EPCs and inhibition of apoptosis of EPCs by SDF-1? and CTCE-0214 will be examined. SDF-1? and CTCE-0214-induced activation of anti-inflammatory pathway and suppression of inflammation will be examined in BMDM and MAECs and by examining CD4+ T cell apoptosis. Such studies may lead to innovative approaches to treat sepsis.
Project Description: As defined in the Award Description field.
Infrastructure Description: N/A
Jobs Summary: None. (Total jobs reported: 0)
Project Status: Not Started
This award's data was last updated on Sep. 28, 2009. Help expand these official descriptions using the wiki below.