Qitao Ran, Ph.D., Assistant Professor
Peking Union Medical College
1995

(210) 562-6129
RAN@UTHSCSA.EDU

Dr. Ran received his PhD degree in Cell Biology from Peking Union Medical College at Beijing in 1995. From 1995 to 2000, Dr. Ran conducted postdoctoral research at Baylor College of Medicine. In 2000, Dr. Ran arrived at Department of Physiology at University of Texas Health Science Center at San Antonio (UTHSCSA) as Assistant Professor/Research. Dr. Ran was appointed Assistant Professor at Department of C&S Biology at UTHSCSA in September of 2006.

Research Interests - The major research interest of Dr. Ran's laboratory is to illustrate the mechanisms of oxidative stress in aging and pathogenesis of Alzheimer's disease. Reactive oxygen species (ROS), which are generated both endogenously and exogenously in living organisms, can damage cellular macromolecules such as protein, DNA and lipid. The imbalance between ROS production and ROS removal/detoxification results in oxidative stress. Oxidative stress is hypothesized to play a causal role in aging and increased oxidative stress is believed to be important in pathogenesis of age-associated diseases such as Alzheimer's disease; however, the mechanisms by which oxidative stress affects these processes remain largely unknown. Polyunsaturated fatty acids, which are found predominantly in membrane lipids, are particularly vulnerable to attack by ROS. Membrane oxidation can damage membrane functions as well as lead to more reactive species production.

Dr. Ran's studies indicate that glutathione peroxidase 4 is an essential antioxidant defense enzyme in protection against membrane oxidation in vivo. Using genetic mouse models with altered antioxidant defense enzymes such glutatione peroxidase 4, Dr. Ran's laboratory is trying to dissect the mechanisms of membrane oxidation in aging and pathogenesis of Alzheimer’s disease. Because mitochondrion is the major source of cellular reactive oxygen species, Dr. Ran’s laboratory is also interested in studying the effect of mitochondrial ROS production and removal on aging and pathogenesis of age-associated diseases using genetic mouse models.

Research Techniques:
Transgenic Mice
Knockout Mice
Gene Expression
Tissue/cell Culture
AD animal models

PUBLICATIONS:
Ran Q, Gu M, Van Remmen H, Strong R, Roberts JL, Richardson A. (2006) Glutathione peroxidase 4 protects cortical neurons from oxidative injury and amyloid toxicity. J Neurosci Res. Jul;84(1):202-8.

Ran Q, Liang H, Gu M, Qi W, Walter CA, Roberts LJ 2nd, Herman B, Richardson A, Van Remmen H. (2004) Transgenic mice overexpressing glutathione peroxidase 4 are protected against oxidative stress-induced apoptosis. J Biol Chem. Dec 31;279(53):55137-46. Epub 2004 Oct 20.

Ran Q, Van Remmen H, Gu M, Qi W, Roberts LJ 2nd, Prolla T, Richardson A. (2003) Embryonic fibroblasts from Gpx4+/- mice: a novel model for studying the role of membrane peroxidation in biological processes. Free Radic Biol Med. Nov 1;35(9):1101-9.

Yant LJ, Ran Q, Rao L, Van Remmen H, Shibatani T, Belter JG, Motta L, Richardson A, Prolla TA. (2003) The selenoprotein GPX4 is essential for mouse development and protects from radiation and oxidative damage insults. Free Radic Biol Med. Feb 15;34(4):496-502.

Ran Q, Pereira-Smith OM. (2000) Identification of an alternatively spliced form of the Tat interactive protein (Tip60), Tip60(beta). Gene. Nov 27;258(1-2):141-6.