Research Activities
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John P. Cooke, MD, PhD |
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The Stanford Program in Vascular Medicine and Biology is enriched by a dynamic and diverse cadre of faculty and research fellows, with broad, deep research expertise in angiogenesis, atherosclerosis, cardiovascular genomics, developmental biology, device development, endothelial biology, epidemiology, genetic models of vascular disease, lipoproteins and metabolism, signal transduction, vascular imaging, vascular physiology and pharmacology.
Opportunities for postdoctoral research are supported by the NHLBI-funded Endothelial Biology (The Cooke Lab)
The focus of our research program is endothelial biology. Ours is a unique research program from “molecule to man” which spans cell and molecular biological studies, as well as preclinical and clinical investigations focused on the role of the NO Synthase pathway in atherogenesis and angiogenesis. We were the first to demonstrate the anti‑atherogenic effects of endothelium-derived Nitric Oxide (EDNO) in animal models. Subsequently we found that EDNO exerts its effects in part by suppressing oxidant‑sensitive transcriptional pathways regulating gene expression of molecules involved in monocyte‑endothelial cell interaction (e.g., VCAM‑1, MCP‑1). Most recently, we have focused on asymmetric dimethylarginine (ADMA) as an endogenous inhibitor of the NOS pathway, and the alterations in ADMA metabolism that occur in atherosclerosis and with risk factors for atherosclerosis.
Another area of interest is in the role of the NOS pathway in angiogenesis. We have investigated the role of ADMA as an endogenous antagonist of angiogenesis. Most recently, we have discovered a novel angiogenic pathway mediated by cholinergic receptors of the nicotinic type ( Heeschen C, et al Nat Med 2001 Jul; 7(7):833-9). This has led to a series of productive investigations in the lab to characterize the cellular and genetic determinants of this pathway.
This work has been enriched by a network of collaborations with other Stanford faculty. Our work is well funded by the National Institutes of Health, the American Heart Association, and other non-profit organizations as well as industry.
Dimethylarginine Dimethylaminohydrolase Overexpression Suppresses Graft Coronary Artery DiseaseMasashi Tanaka, Karsten Sydow, Feny Gunawan, Johannes Jacobi, Phil S. Tsao, Robert C. Robbins and John P. Cooke Circulation 2005;112;1549-1556; originally published online Sep 6, 2005;
