Associate Professor, Department of Molecular and Cellular Physiology

Contact Information:
Email: Office Phone: 318-675-8420
Office Fax: 318-675-6005

Postdoctoral Training, Physiology, 1998-2004, LSUHSC-Shreveport
Ph.D., Physiology, 2004, Trinity College, Dublin, Ireland
B.A. Mod., Physiology , 1993, Trinity College, Dublin, Ireland

Major Research Interests:  
The Inflammatory Impact of Cytomegalovirus on the Microvasculature

Inflammation is a key player in the pathogenesis of cardiovascular disease. In the case of several cardiovascular risk factors, including hypercholesterolemia, clinical signs of disease are preceded by the development of an inflammatory phenotype in the microvasculature, which may promote a low-grade systemic inflammation rendering tissues more susceptible to injurious stimuli or other risk factors. Recent epidemiological studies have revealed that infectious agents, for example cytomegalovirus (CMV), may contribute to cardiovascular disease. CMV is a beta-herpesvirus that has been identified in atherosclerotic lesions, and accelerates disease progression in hyperlipidemic animals. CMV induces an inflammatory phenotype in isolated cells. Our findings show that CMV also induces endothelial dysfunction in arterioles in vivo, and exacerbates hypercholesterolemia-induced blood cell recruitment in postcapillary venules. Therefore our focus is to investigate the underlying mechanisms involved in the microvascular responses to CMV, and its cooperation with other cardiovascular risk factors in the generation of a pro-inflammatory phenotype. Some of our areas of interest include the role of platelets, reactive oxygen species and cytokines.

Representative Publications:

Jiang B, Hebert VY, Khandelwal AR, Stokes KY, Dugas TR. HIV-1 antiretrovirals induce oxidant injury and increase intima-media thickness in an atherogenic mouse model. Toxicol Lett. 2009;187(3):164-71. PMCID: PMC2680796.


Khoretonenko MV, Leskov IL, Jennings SR, Yurochko AD, Stokes KY. Cytomegalovirus infection leads to microvascular dysfunction and exacerbates hypercholesterolemia-induced responses. Am J Pathol. 2010;177(4):2134-44. PMCID: PMC2947306.


Yilmaz G, Vital S, Erkuran Yilmaz C, Stokes KY, Alexander SJ, Granger DN. Selectin-mediated recruitment of bone marrow stromal cells in the postischemic cerebral microvasculature. Stroke. 2010; 42(3):806-11. PMCID: PMC3042505.


Senchenkov E, Khoretonenko MV, Leskov IL, Stokes KY. P-selectin is upregulated by cytomegalovirus infection and mediates the associated microvascular dysfunction. Microcirculation. 2011;18(6):452-62. PMCID: PMC3148337.


Leskov IL, Stokes KY. Cytomegalovirus infection promotes microvascular dysfunction through an NAD(P)H oxidase-dependent pathway Free Radic Biol Med 2011;51(12):2300-8. PMCID: PMC3272703.


Stokes KY, Granger DN. Platelets: A critical link between inflammation and microvascular dysfunction. J Physiol. 2012;590(Pt 5):1023-34. PMCID: PMC3381810.


Singer G, Stokes KY, Granger DN. Reactive oxygen and nitrogen species in sepsis-induced hepatic microvascular dysfunction. Inflamm Res. 2013;62(2):155-64.40.      


Palaniyandi S, Radhakrishnan SV, Karlsson FJ, Stokes KY, Kittan N, Huber E, Hildebrandt GC. Murine cytomegalovirus immediate-early 1 gene expression correlates with increased GVHD after allogeneic hematopoietic cell transplantation in recipients reactivating from latent infection. PLoS ONE. 2013;8(4):e61841.