Phosphoinositide-Driven Epithelial Proliferation in Prostatic Inflammation
Annual summary rept. 1 Jan 2007-31 Mar 2009
Pagination or Media Count:
With this proposal, we seek to determine the mechanisms for epithelial proliferation in response to inflammation, a process termed reactive hyperplasia. The purpose of this report is to evaluate the first year of research on this project. We found that interleukin signaling is critical to the hyperplastic response of the prostate, and that proliferation is driven in the epithelium of the prostate by phosphoinositide-dependent action, while stromal proliferation appears dependent on Jak-STAT signaling. We expanded this project in response to a startling discovery a myriad of inflammatory mediators are expressed at high levels during organogenesis of the prostate, a process that, like reactive hyperplasia, is characterized by rapid epithelial proliferation. We found the interleukin-1 signaling is critical to epithelial proliferation during organogenesis. Future research will determine the mechanisms of IL-1 action in development and reactive hyperplasia in the prostate.
- Medicine and Medical Research