Overview

Education
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
Pharmacology (1974)
Professional Activities and Honors
Chairman/member, AHA Peer Review Subcommittee, Research Program and Evaluation
Committee (1997-2000)
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
Physiology (1989-Present)
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,

Education

PHD, 1974, Duke University
PHD, 1965, Catholic University of Chile

Languages

Spanish

Relevant Publications

1. Aguilar G, Cordova F, Koning T, Boric MP, Birukov K, Cancino J, Varas-Godoy M, Soza A, Alves NG, Mujica PE, Duran WN, Ehrenfeld P, Sanchez FA. (2021). TNF-a activated eNOS signaling increases leukocyte adhesion through the S-nitrosylation pathway. Am J Physiol: Heart & Circulatory Physiology. 321: H1083-H1095.

2. Guequen A, Zamorano P, Cordova F, Koning T, Torres A, Ehrenfeld P, Boric MP, Salazar-Onfray F, Gavard J, Duran WN, Quezada C, Sarmiento JM, Sanchez FA. (2019). Interleukin-8 secreted by glioblastoma cells induces microvascular hyperpermeability through NO signaling involving S- nitrosylation of VE-cadherin and p120 in endothelial cells. Front. Physiol. Vol 10: pp. 1-12.

3. Ehrenfeld P, Cordova F, Duran WN, Sanchez FA. (2019). S-nitrosylation and its role in breast cancer angiogenesis and metastasis. Nitric Oxide 87:52-59.

4. Korayem AH, Mujica PE, Aramoto H, Duran RG, Nepali PR, Kim DD, Harris AL, Sanchez FA and Duran WN (2017). Endothelial cAMP deactivates ischemia/reperfusion-induced microvascular hyperperme-ability via Rap1-mediated mechanisms. Am J Physiol: Heart & Circ Physiol. 313: H179 - H189.

5. Zamorano P, Marin N, Cordova F, Aguilar A, Meininger C, Boric MP, Golenhofen N, Contreras J, Sarmiento J, Duran WN, Sanchez FA (2017). S-nitrosylation of VASP at cysteine 64 mediates inflammation stimulated increase in microvascular permeability. Am J Physiol: Heart & Circ Physiol. 313: H66 - H71.

6. Crawford JM, Lal BK, Duran WN, Pappas PJ. (2017) Pathophysiology of venous ulceration. J Vasc Surg Ven Lymph Dis. 5: 596 - 605.

7. 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.

8. Duran WN, Sanchez FA. (2016). New member of endothelial arsenal against inflammation. Circ. Res. 19:178-180.

9. 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.

10. Duran WN, Beuve AV, Sanchez FA. (2013). Nitric oxide, S-nitrosation and endothelial permeability. IUBMB Life. 65:819-826. Complete List of Published Work - See links Tab

Course List

DENT5065Q

Dental Physiology

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.