I have been studying endothelial cell biology in health and disease;
in particular itâ€™s response under conditions that influence the
accelerated-atherosclerotic process seen in diabetic arteries. Results reported
from my laboratory have demonstrated the profound involvement of endothelial
nitric oxide synthase under hyperglycemic conditions. My current studies are
focused toward determining how the balance of activities of Inhibitor kappa B
kinase and endothelial nitric oxide synthase reflect oxidative stress responses
of endothelial cells that are induced by high glucose and alter vessel
remodeling after arterial injury. Also, generation of a double knockout mouse
(eNOS knockout mouse with a diabetic background) and diabetic mouse
overexpressing eNOS in the blood vessels in my laboratory will illuminate some
of the basic mechanisms in vivo.
Yu H, Mohan S, Natarajan M. Radiation-Triggered NF-ÎºB Activation is Responsible for the Angiogenic Signaling Pathway and Neovascularization for Breast Cancer Cell Proliferation and Growth. Breast Cancer (Auckl). 2012;6:125-35.
Zheng X, Mohan S, Otto RA, Natarajan M. Endothelial cell migration was impaired by irradiation-induced inhibition of SHP-2 in radiotherapy: an in vitro study. J Radiat Res. 2011;52(3):320-8.
Mohan S, Konopinski R, Yan B, Centonze VE, Natarajan M. High glucose-induced IKK-Hsp-90 interaction contributes to endothelial dysfunction. Am J Physiol Cell Physiol. 2009 Jan;296(1):C182-92.
Mohan S, Reddick RL, Musi N, Horn DA, Yan B, Prihoda TJ, Natarajan M, Abboud-Werner SL. Diabetic eNOS knockout mice develop distinct macro- and microvascular complications. Lab Invest. 2008 May;88(5):515-28.
Mohan S, Koyoma K, Thangasamy A, Nakano H, Glickman RD, Mohan N. Low shear stress preferentially enhances IKK activity through selective sources of ROS for persistent activation of NF-kappaB in endothelial cells. Am J Physiol Cell Physiol. 2007 Jan;292(1):C362-71.