Qing Guo, MD, PhD

Dr. Guo is Professor of Physiology at the University of Oklahoma Health Sciences Center (OUHSC), College of Medicine. He is also a faculty member in the Physiology and Neuroscience Graduate Programs at OUHSC.

Education and Training: 
Dr. Guo received his M.D. degree in medicine in 1984 and Ph.D. in neurobiology in 1993. He pursued postdoctoral research in molecular biology of cell death under Professor Mark P. Mattson in Sanders-Brown Center on Aging at the University of Kentucky before joining the faculty in the Department of Neurobiology and Pharmacology at Northeastern Ohio Universities College of Medicine (NEOUCOM) in 1999.  Since 2003, Dr. Guo has been a faculty member in the Department of Physiology at the University of Oklahoma Health Sciences Center.

Resarch Summary: Signaling of Cell Death in Physiology and Disease
Research in Dr. Guo's laboratory centers on some of the fundamental questions in the life and death of cells in a variety of organ systems and diseases, particularly those related to neuronal injury and neurodegeneration. First, we examine how specific genetic mutations and cell death proteins regulate intracellular pathways that control cellular life and death. Secondly, we examine how aberrant regulation of the apoptotic machinery is involved in pathological disease conditions, such as neurodegeneration, brain trauma, and acute renal failure. Our studies involve the application of a variety of gene transfer and targeting protocols, including the generation and characterization of transgenic and/or knockin/knockout mouse models. Dr. Guo has served on NIH study sections and reviews grant applications for national and international funding agencies. He also serves on Editorial Boards of several professional journals and reviews manuscripts on a regular basis.

Teaching and Mentoring:
Dr. Guo's teaching experience began in 1984, and he has taught students of different academic, ethnic and economical backgrounds, with diverse career goals and personal interests. Dr. Guo's lectures and lab sessions covered ma
ny topics including those in Medical Neuroscience, Functional Neuroanatomy, Medical Physiology (including respiratory physiology), Medical Problems, Cell Death in Physiology and Disease, Mechanisms of Aging, Reproduction and Women's Health, and Journal Clubs. He was the course director for Integrative Physiology, a core course for graduate students in Graduate Programs in Biomedical Sciences (GPiBS) at OUHSC. He also served as Chair of graduate programs in Physiology at OUHSC. He had the pleasure of mentoring seven PhD students in his lab. Beyond his own laboratory, he served on many PhD dissertation committees, covering campuses of Northeastern Ohio Universities College of Medicine and Pharmacy (NEOUCOM), OUHSC and Oklahoma Medical Research Foundation (OMRF). 

Selected Publications:
  • Najeeb A Shiwany, Jun Xie and Qing Guo. Cortical neurons transgenic for human Aβ40 or Aβ42 have similar vulnerability to apoptosis despite their different amyloidogenic properties. Int J Clin Exp Pathol  2(4);  2009; 339-352.
  • Daniel J. Payette, Jun Xie, Najeeb Shirwany, and Qing Guo. Exacerbation of apoptosis of cortical neurons following traumatic brain injury in Par-4 transgenic mice. Int J Clin Exp Pathol  2008; 1: 44-56
  • Najeeb A Shirwany, Daniel Payette, Jun Xie, and Qing Guo. The amyloid beta ion channel hypothesis of Alzheimer’s disease: A review. Neuropsychiatric Disease and Treatment. 2007: 3(5) 597-612.
  • Jun Xie, and Qing Guo. Par-4 is Novel Mediator of Renal Tubule Cell Death in Models of Ischemia-Reperfusion Injury. Am. J. Physiol. Renal Physiol., 2007; 292(1): F107-F115.
  • Jun Xie, and Qing Guo.  Apoptosis Antagonizing Transcription Factor Protects Renal Tubule Cells against Oxidative Damage and Apoptosis Induced by Ischemia-Reperfusion. J. Am. Soc. Nephrol. 2006; 17(12): 3336-3346.
  • Jun Xie, and Qing Guo. Par-4 Is involved in regulation of beta -secretase cleavage of the Alzheimer’s amyloid precursor protein. J Biol Chem., 2005; 280(14): 13824-13832.  
  • Jun Xie, Keytam S. Awad, and Qing Guo. RNAi knockdown of Par-4 inhibits neurosynaptic degeneration in ALS-linked mice. J Neurochem. 2005; 92, 59-71.
  • Jun Xie, and Qing Guo. AATF protects neural cells against oxidative damage induced by amyloid beta-peptide. Neurobiol Dis  2004; 16, 150-157.
  • Jun Xie, and Qing Guo. Par-4 inhibits choline uptake by interacting with CHT1 and reducing its incorporation on the plasma membrane. J Biol Chem 2004; 279, 28266-28275.
  • Qing Guo, and Xie, J. AATF inhibits aberrant production of amyloid beta peptide 1-42 by interacting directly with Par-4. J Biol Chem 2004; 279, 4596-4603
  • Qing Guo, Jun Xie, Xiaowei Chang, and Huimin Du. Prostate Apoptosis Response-4 Enhances Secretion of Amyloid beta Peptide 1-42 in Human Neuroblastoma IMR-32 Cells by a Caspase-dependent Pathway.  J. Biol. Chem. 2001; 276: 16040-16044
  • Qing Guo, Weiming Fu, Bryce Sopher, Miles W. Miller, Carol B. Ware, George M. Martin, and Mark P. Mattson. Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice. Nature Medicine  1999; 5: 101-107.
  • Qing Guo, Lois Sebastian, Bryce Sopher, Miles W. Miller, Gordon W. Glazner, Carol B. Ware, George M. Martin, and Mark P. Mattson.  Neurotrophic factors (ADNF and bFGF) interrupt excitotoxic neurodegenerative cascades promoted by a PS1 mutation.  Proc. Natl. Acad. Sci. USA. 1999; 96(7): 4125-4130
  • Qing Guo, Weiming Fu, Jun Xie, Hong Luo, Stephen J. Sells, James W. Geddes, Vimala Bondada, Vivek M. Rangnekar and Mark P. Mattson.  Par-4 is a new mediator of neuronal degeneration associated with the pathogenesis of Alzheimer’s disease.  Nature Medicine  1998; August, 4(8): 957-962
  • Qing Guo, Sylvia Christakos, Nic Robinson and Mark P. Mattson.    Calbindin D28K Blocks the Pro-Apoptotic Actions of Mutant Presenilin-1:  Reduced Oxidative Stress and Preserved Mitochondrial Function. Proc. Natl. Acad. Sci. USA. 1998; 95:3227-3232.
  • Qing Guo, Nic Robinson and Mark P. Mattson.  Secreted beta-amyloid precursor protein counteracts the pro-apoptotic action of mutant presenilin-1 by activation of NF-kB and stabilization of calcium homeostasis.   J. Biol. Chem. 1998; 273 (20): 12341-12351.
  • Jeffrey N. Keller, Qing Guo, F.W. Holtsberg, A.J. Bruce-Keller, and Mark P. Mattson.  Increased sensitivity to mitochondrial toxin-induced apoptosis in neural cells expressing mutant presenilin-1 in linked to perturbed calcium homeostasis and enhanced oxyradical production.   J. Neurosci.  1998; 18(12):  4439-4450.
  • Qing Guo, Bryce L. Sopher, Katsutoshi Furukawa, Dao G. Pham, George M. Martin and Mark P. Mattson.  Alzheimer's PS-1 mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid beta-peptide: Involvement of calcium and oxyradicals.   J. Neurosci. 1997; 17(11): 4212-4222
  • Ward A. Peterson, Qing Guo, Boyd K. Hartmans, and Mark P. Mattson. Nerve growth factor-independent reduction in choline acetyltransferase activity in PC12 cells expressing mutant presenilin-1.  J. Biol. Chem. 1997; 272(36): 22397-22400
  • http://find.ouhsc.edu/Faculty.aspx?FacultyID=744

Funding Agencies:

  • National Institutes of Health
  • Alzheimer’s Association
  • ALS Association
  • American Federal for Aging Research
  • Harold Hamm Diabetes Center
  • Oklahoma Center for the Advancement of Science and Technology (OCAST)

Phone: (405) 271-2226 ext. 56268
Mailing Address: Department of Physiology, The University of Oklahoma Health Sciences Center, 940 Stanton L. Young Blvd., BMSB Rm. 607, Oklahoma City, Oklahoma 73104 U.S.A.