442 PHARMACY BUILDING
881 MADISON AVENUE
MEMPHIS TN 38163
- PostDoc, Stanford University, Gene Therapy
- Ph.D., Medical College of Wisconsin, Physiology
Download My Curriculum Vitae
My lab focuses on the role of Activator of G-protein Signaling, a family of accessory proteins, in renal epithelial cell repair. Upon injury to the kidney by biological insults (eg. ischemia-reperfusion injury or chemicals) or genetic damage, the renal epithelial cells undergo a well orchestrated set of steps to initiate repair of the damaged cells. Due to the importance of G-proteins in this process, our lab has identified novel accessory proteins that can control the activation/inactivation of specific G-protein subunits, specifically AGS3 or GPSM1, to mediate this reparative response in mouse models of renal injury.
At this time, we have discovered that AGS3 can play a critical role in the repair of the renal epithelial cell following ischemia-reperfusion injury. In the absence of AGS3, the renal epithelial cells are unable to fully recover from the ischemia-reperfusion related damage to the kidney. Subsequently, we discovered that AGS3 is abnormally expressed in mouse models of polycystic kidney disease, which can be a system to evaluate "futile" repair mechanisms, since the genetic mutations do not allow the kidney to return back to normal and lead to the formation of renal cysts. In these models, the loss of AGS3 resulted in exacerbated cystic disease progression.
Because of these initial findings regarding the role of AGS proteins in the kidney, our lab is now studying the role of other AGS proteins and how their expression profiles relate to the repair of the renal epithelial cells in the kidney.
Accessory proteins, Activator of G-protein signaling, kidney, acute kidney injury, polycystic kidney disease, lentiviral vectors
- Kwon, M, Pavlov, TS, Nozu, K, Rasmussen, SA, Ilatovskaya, DV, Lerch-Gaggl, A, North, LM, Kim, H, Qian, F, Sweeney, WE, Avner, ED, Blumer, JB, Staruschenko, A, Park, F. G-protein signaling modulator 1 deficiency accelerates cystic disease in an orthologous mouse model of autosomal dominant polycystic kidney disease. Proc Natl Acad Sci U S A, 109 (52), 21462-7, 2012.
- Regner, KR, Nozu, K, Lanier, SM, Blumer, JB, Avner, ED, Sweeney, WE, Park, F. Loss of activator of G-protein signaling 3 impairs renal tubular regeneration following acute kidney injury in rodents. FASEB J, 25 (6), 1844-55, 2011.
- Roman, RJ, Akbulut, T, Park, F, Regner, KR. 20-HETE in acute kidney injury. Kidney Int, 79 (1), 10-3, 2011.