Yafeng Dong, PhD

Associate Professor, Department of Obstetrics and Gynecology
PhD: Department of Physiology, Xian Medical University, China
Postdoctoral: University of Maryland School of Medicine

Publications: Click here

Personal History

I completed my undergraduate and graduate studies and received my PhD through the Department of Physiology at Xian Medical University, China. Postdoctoral training was obtained in the laboratory of Dr. Marc Simard and Dr. Loren Thompson at University of Maryland School of Medicine. In 2006, I joined the faculty of the Department of Obstetrics and Gynecology at University of Kansas School of Medicine.  

Research Interests

The problem of perinatal brain injury, in terms of the costs to society and to the affected individuals and their families, is extraordinary. The most common underlying cause of perinatal brain injury is hypoxia/ischemia.  Intrauterine hypoxia and birth asphyxia induced brain damage are associated with increased perinatal mortality and long term sequelae of neurodevelopmental compromise, seizures disorders and cerebral palsy.  The roles of ROS, Ca2+, NMDA receptors, excitatory amino acids, and apoptotic genes on fetal brain injury have been studied exclusively. These works have led to substantial conceptual agreement on a general outline of how fetal brain injury triggers and evolves to produce neuropathologic lesions and neurodevelopmental disabilities. However, the precise etiological factors for the development of the majority of fetal hypoxic brain injury have not been identified satisfactorily. We initially indicated that multiple pathways involved in the fetal brain injury mediated by chronic hypoxia.

Role of proinflammation cytokine in fetal brain injury during chronic hypoxia: Our studies reveal an association between fetal hypoxemia damage and a marked inflammatory reaction that contributes to the tissue injury.  With the approach of gene microarray and quantitation PCR techniques, we indicated that degrees of hypoxia induced stress created fetal organ damage via up regulation fetal pro-inflammatory cytokines; pro-inflammatory cytokines play a central role in the causation of fetal organ damage in hypoxia condition. However, the specific mechanism underlying these processes is poorly understood. The ultimate goal of our lab is to study the molecular mechanism of pro-inflammatory cytokine regulation in hypoxemia fetus.

Proteomic identification of specific proteins by chronic hypoxia in fetal organ damage: By utilizing advanced proteomic techniques, we found, a new novel protein, phosphorylated cofilin-1 dramatically down regulated in hypoxic fetal brain, and cofilin-1 post translational modification (phosphorylation), mediated by reactive oxygen species(ROS), involved in the novel mechanism of the fetal hypoxic brain damage. We hypothesize that chronic hypoxia induces the cofilin gene modification mediated by ROS. Dephosphorylated cofilin may evoke activation of apoptotic genes leading to neuronal damage in the preterm hypoxic fetal brain. Further studies will be performed, we hope the findings may provide a new concept resulting in the development of a pharmacological inhibitor to inactivate cofilin and prevent chronic hypoxia, which would have a major impact and implication on brain injuries in the fetus.

Lab Techniques and Equipment

Research Techniques 

  1. Histology and Imaging: Immunocytochemistry; Confocal microscopy, Laser microdissection capture.
  2. Molecular biology: Molecular cloning; Southern and Northern blot analysis; cDNA library construction; Quantitative RT-PCR; In situ hybridization; Gene MicroArray; siRNA.
  3. Biochemistry: Protein isolation and purification; Protein differential fractionation; Co-Immunoprecipitation; 2-dimensional gel electrophoresis; MALDI-TOF; LC/MS/MS; Western blotting; RIA; ELISA assays, Phosphorylation assays.  
  4. Cell and tissue culture: primary neuronal cell; neuron or astrocyte cell line culture; transfection of cells and tissues.


  • Dr. Carl P. Weiner: Pregnancy effect on vascular smooth muscle/endothelium.
  • Dr. Michael J. Soares: Chronic hypoxia effect on fetus development.
  • Dr. Antonio Artigues: Proteomic identification of specific proteins by chronic  hypoxia in fetal organ damage.  

Laboratory Personnel

The laboratory has several openings for technicians, and postdoctoral fellows. Please email your CV/resume.

Current Personnel

  • Qing Zhu, Ph.D., Post-doctoral research fellow
  • Weijian Hou, Ph.D., Research Associate
  • Josh Sites, B.S., Research Assistant


  1. Lin RX,  Roseborough G, Dong Y, Williams M, and Wei CM  2003  DNA damage and repair system in spinal cord ischemia. Journal of Vascular Surgery 37(4), 847-858.
  2. Dalton S, Gerzanich V, Chen M, Dong Y, Shuba Y, and Simard JM 2003 Chlorotoxin-sensitive Ca2+-activated Cl- channel in type R2 reactive astrocytes from adult rat brain. Glia 42, 325-339.
  3. Murphy K, Gerzanich V, Zhou H, Ivanova S, Dong Y, Hoffman G, Alexander WG, Winn HR, and Simard JM  2003 Adenosine-A2a receptor down-regulates cerebral smooth muscle L-type Ca2+ channel activity via protein tyrosine phosphatase, not camp-dependent protein kinase. Molecular Pharmacology 64(3), 640-649.
  4. Chen M, Dong Y, and Simard JM 2003 Functional coupling between sulfonylurea receptor-1 and non-selective cation channel in reactive astrocytes from adult rat brain. The Journal of Neuroscience 24, 8568-8577.
  5. Gerzanich V, Ivanov A, Ivanova S, Yang JB, Zhou H, Dong Y 2003 Alternative splicing of cGMP-dependent protein kinase I in angiotensin-hypertension novel mechanism for nitrate tolerance in vascular smooth muscle. Circulation Research 93(9), 805-812.
  6. Thompson LP, Dong Y 2005 Chronic hypoxia decreases endothelial nitric oxide synthase protein expression in fetal guinea pig hearts. J Soc Gynecol Investig 12(6), 388-395.
  7. Dong Y, Thompson LP. 2006 Differential expression of endothelial nitric oxide synthase in coronary and cardiac tissue in hypoxic fetal guinea pig hearts. J. Soc Gynecol Investig 13(7), 483-90
  8. Yafeng Dong, Daqing Gao, Lei Chen, Ruxian Lin, John V.Conte and Chiming Wei. Increased ERK activation and decreased MKP-1 expression in human myocardium with congestive heart failure. Journal of Cardiothoracic-Renal Research. 2006 1(2): 123-130
  9. Vladimir V Yurosky, Volodymyr Gerzanich, Svetlana Ivanova, Yafeng Dong, Orest Tsymbalyuk, J Marc Simard. 2007 Autocrine TGF-beta(1) Mediates Angiotensin II-induced Proliferative Response of Cerebral Vessels In Vivo. Am J Hypertens. 20(9): 950-956.
  10. Oh C, Dong Y, Harman C, Mighty HE, Kopelman J, Thompson LP. 2008 Chronic hypoxia differentially increases glutathione content and gamma-glutamyl cysteine sythetase expression in fetal guinea pig organs. Early Hum Dev, Feb; 84(2):121-7
  11. Chien Oh, Yafeng Dong, Hongshan Liu, Loren P Thompson. 2008 Intrauterine hypoxia upregulates  proinflammatory cytokines and matrix metalloproteinases in fetal guinea pig hearts. Am J Obstet Gynecol. Feb 14;[Epub ahead of print] PMID: 18279828

Last modified: Sep 24, 2013

Yafeng Dong, PhD, Associate Professor


Yafeng Dong, PhD
Associate Professor, Department of Obstetrics and Gynecology