CSB Faculty

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:
Chen L, Na R, Gu M, Richardson A, Ran Q. (2008) Lipid peroxidation up-regulates BACE1 expression in vivo: a possible early event of amyloidogenesis in Alzheimer's disease. J Neurochem. 2008 Oct;107(1):197-207. Epub 2008 Aug 2.

Chen L, Na R, Gu M, Salmon AB, Liu Y, Liang H, Qi W, Van Remmen H, Richardson A, Ran Q. (2008) Reduction of mitochondrial H(2)O(2) by overexpressing peroxiredoxin 3 improves glucose tolerance in mice. Aging Cell. 2008 Sep 5.

Guo Z, Ran Q, Roberts LJ 2nd, Zhou L, Richardson A, Sharan C, Wu D, Yang H. (2008) Suppression of atherogenesis by overexpression of glutathione peroxidase-4 in apolipoprotein E-deficient mice. Free Radic Biol Med. 2008 Feb 1;44(3):343-52. Epub 2007 Oct 2.

Liang H, Van Remmen H, Frohlich V, Lechleiter J, Richardson A, Ran Q. (2007) Gpx4 protects mitochondrial ATP generation against oxidative damage. Biochem Biophys Res Commun. 2007 May 18;356(4):893-8. Epub 2007 Mar 21.

Ran Q, Liang H, Ikeno Y, Qi W, Prolla TA, Roberts LJ 2nd, Wolf N, Van Remmen H, Richardson A. (2007) Reduction in glutathione peroxidase 4 increases life span through increased sensitivity to apoptosis.
J Gerontol A Biol Sci Med Sci. 2007 Sep;62(9):932-42.