Pontificia Universidad Catolica de Chile, Facultad de Filosofia y Ciencias de la
Educacion, Profesor de Biologia (1965)
Duke University Graduate School of Arts and Sciences, Ph.D. in Physiology and
Professional Activities and Honors
Chairman/member, AHA Peer Review Subcommittee, Research Program and Evaluation
Member, Awards Committee, American Physiological Society (APS) (1999 ? 2003)
Chairman, Fellowship Committee, Cardiovascular Section, APS (1998-2001)
President, The Microcirculatory Society (2000-2001)
1995 UMDNJ University Excellence Award in Biomedical Research
1983 ? 1988 Established Investigator of the American Heart Association
Associate Editor/Editorial Board member, Microvascular Research (1984 - Present)
Editorial Board member, American Journal of Physiology: Heart & Circulatory
Editorial Board Member, World Journal of Traditional Chinese Medicine (2014-Present)
Editorial Board member, Circulation Research (2012 - Present)
Member, Experimental Cardiovascular Sciences Study Section, Center for Scientific
Review, National Institutes of Health (1990? 1994)
Member, Pharmacology/Hypertension and Microcirculation Study Section,
Ph.D., 1974, Duke University Ph.D., 1965, Catholic University of Chile
1. Guequen A, Carrasco R, Zamorano P, Rebolledo L, Burboa P, Sarmiento J, Boric MP, Korayem A, Duran WN, Sanchez FA. (2016). S-nitrosylation regulates VE-cadherin phosphorylation and internalization in microvascular permeability. Am. J. Physiol.: Heart Circ. Physiol. 310: H1039 ? 1044.
2. Deitch EA, Condon M, Feketeova E, Machiedo GW, Mason L, Vinluan G, Vamsi A, Tomaio JN., Fishman JE, Duran WN, Spolarics Z. (2014). Trauma-hemorrhagic shock induces a CD36-dependent RBC endothelial-adhesive phenotype. Crit Care Med 42(3):e200-e210.
3. Duran WN, Beuve AV, Sanchez FA. (2013). Nitric oxide, S-nitrosation and endothelial permeability. IUBMB Life. 65:819-826
4. Marin N, Zamorano P, Carrasco R, Mujica P, Gonzalez FG, Quezada C, Meininger CJ, Boric MP, Duran WN, Sanchez FA. (2012) S-nitrosation of B-catenin and p120 catenin: a novel regulatory mechanism in endothelial hyperpermeability. Circ. Res. 11: 553-563.
5. Crassous PA, Couloubaly S, Huang C, Zhou Z, Baskaran P, Kim DD, Papapetropoulos A, Fioramonti X, Duran WN, Beuve A. (2012). Soluble guanylyl cyclase is a target of angiotensin II-induced nitrosative stress in a hypertensive rat model. Am J Physiol Heart Circ Physiol. 303:H597-H604.
6. Sanchez, FA, Rana R, Gonzalez FG, Iwahashi T, Duran RG, Fulton DJ, Beuve AV, Kim DD, Duran WN. (2011). Functional significance of cytosolic eNOS: Regulation of hyperpermeability. J Biol Chem. 286:30409-30414
7. Duran WN, Breslin JW, Sanchez FA. (2010). The NO cascade, eNOS location, and microvascular permeability. Cardiovasc Res. 87:254-261.
8. Sanchez FA, Rana R, Kim DD, Iwahashi T, Zheng R, Lal BK, Gordon DM, Meininger CJ, Duran WN. (2009). Internalization of eNOS and NO delivery to subcellular targets determine agonist-induced hyperpermeability. Proc Natl Acad Sci. 106: 6849?6853.
9. Sayed N, Kim DD, Fioramonti X, Iwahashi T, Duran WN, Beuve A. (2008) Nitroglycerin-induced S-nitrosylation and desensitization of soluble guanylyl cyclase contribute to nitrate tolerance. Circ Res 103:606-614.
10. Hatakeyama T, Pappas PJ, Hobson II RW, Boric MP, Sessa WC, Duran WN. (2006). Endothelial nitric oxide synthase regulates microvascular hyperpermeability in vivo, J Physiol. (London) 574: 275-281.
Complete List of Published Work see links Tab
Regulatory Signaling Pathways In Microvascular Permeability
The main function of the cardiovascular system is to support cell life through the exchange of solutes across microvascular walls. We investigate the signaling pathways that regulate microvascular permeability using in vivo as well as in vitro molecular biology approaches. We have demonstrated that endothelial nitric oxide synthase (eNOS) is fundamental for promoting hyperpermeability in response to pro-inflammatory agents. We also showed that traffic of eNOS from its location in the cell membrane (caveolae) to the cytosol is a fundamental requirement in order to cause the onset of hyperpermeability, and that S-nitrosylation of junctional proteins is an important mechanism for increasing endothelial microvascular permeability. We are currently investigating mechanisms of deactivation of inflammation-promoted hyperpermeability. In terms of translational research, we are investigating the mechanisms that terminate hyperpermeability in ischemia-reperfusion injury.