Shi Pan, Ph.D.
See information for Patients. Viewing information for Researchers.
Contact
University of Rochester
School of Medicine and Dentistry
601 Elmwood Ave, Box CVRI
Rochester, New York 14642
Office: 585 276-9790 (Ext. 69790) (primary)
Lab: 585 276-9846
Fax: 585 276-9830
Reactive oxygen species (ROS) are generated in all aerobic organisms as the result of normal cellular metabolism. A balance of generating and neutralizing processes establishes the redox homeostasis, which is important for normal cell function. Alteration of the redox homeostasis by the increased generation of ROS is implicated in the pathophysiology of a variety of vascular diseases, including coronary artery disease, arrhythmias, congestive heart failure, cardiomyopathy, atherosclerosis, hypertension, ischemia-reperfusion injury and diabetes.
The intracellular milieu is usually a reduced environment resulting from a high concentration of glutathione. In cells experiencing oxidative stress, a continual supply of reducing equivalents in the form of NADPH is required, which is provided by pentose phosphate pathway. Glutathione protects cells against ROS through a variety of mechanisms by using NADPH as a reducing power.
When exposed to ROS, reactive-thiol-containing proteins undergo certain post-translational modifications. One of them is S-glutathionylation, the formation of glutathione-mixed disulfide bond, which protects protein from loss of function caused by irreversible oxidation. Glutathionylated proteins contain cytoskeletal proteins, signaling molecules including phosphatases and kinases, and transcription factors, which indicates that glutathionylation is an important mechanism that links the changes in the intracellular redox potential to the regulation of protein function.
The aim of Dr. Pan's research is to understand the redox regulation of cardiovascular function. These studies will be a critical step in determining the molecular mechanisms as well as targets to the treatment of cardiovascular diseases.
Current Appointments
- Assistant Professor - Department of Medicine, Aab Cardiovascular Research Institute (SMD)
| Education | ||
|---|---|---|
| PhD Molecular and Cellular Biology | University of Tokyo | 1998 |
| Masters Genetics | Northeast Forestry University | 1990 |
| Bachelors Biology | Northeast Normal University | 1985 |
| Post-Doctoral Training & Residency | |
|---|---|
| University of Pittsburgh, Pittsburgh, PA | 2000 - 2002 |
| University of Tokyo, Tokyo, Japan | 1998 - 2000 |
| Fellowship Awards | |
|---|---|
| Japanese Ministry of Education, University of Tokyo | 1993 - 1998 |
Lab Description
Research * TNF/Redox regulation of endothelial function during inflammation and atherosclerosis.
Lab Website
http://www.urmc.rochester.edu/cvri/research/berk-lab.cfm
| Recent Journal Articles |
|---|
| Showing the 5 most recent journal articles. (11 available) |
| Satoh, K.; Matoba, T.; Suzuki, J.; O'Dell, MR.; Mohan, A.; Pan, S.; Li, L.; Jin, ZG.; Abe, J.; Berk, BC. "Cyclophilin A mediates vascular remodeling by promoting inflammation and vascular smooth muscle cell proliferation." Circulation (2008). |
| Pan S; Berk BC. "Glutathiolation regulates tumor necrosis factor-alpha-induced caspase-3 cleavage and apoptosis: key role for glutaredoxin in the death pathway." Circulation research. 2007; 100(2):213-9. Epub 2006 Dec 21. |
| Wang J; Pan S; Berk BC. "Glutaredoxin mediates Akt and eNOS activation by flow in a glutathione reductase-dependent manner." Arteriosclerosis, thrombosis, and vascular biology. 2007; 27(6):1283-8. Epub 2007 Apr 12. |
| Yamawaki H; Pan S; Lee RT; Berk BC. "Fluid shear stress inhibits vascular inflammation by decreasing thioredoxin-interacting protein in endothelial cells." The Journal of clinical investigation. 2005; 115(3):733-8. |
| Tai LK; Zheng Q; Pan S; Jin ZG; Berk BC. "Flow activates ERK1/2 and endothelial nitric oxide synthase via a pathway involving PECAM1, SHP2, and Tie2." The Journal of biological chemistry. 2005; 280(33):29620-4. Epub 2005 Jun 28. |
