The University of Toledo

Guillermo Vazquez

Associate Professor Phone: (419) 383-5301 Fax: (419) 383-2871 E-mail: Guillermo.Vazquez@utoledo.edu

Training:

BSc Biochemistry, 1990, National University of the South, Argentina
PhD Biochemistry, 1997, National University of the South, Argentina
Postdoctoral Fellow, 1997, Argentinean National Research Council (CONICET) 
Postdoctoral Fellow, 2001-2005: NIEHS, North Carolina, USA
Research Fellow, 2006: NIEHS, North Carolina, USA

Appointments:

• Member of the Scientific and Technological Researcher Career, CONICET, Argentina  1997-2004.
• Visiting Postdoctoral Fellow, Calcium Regulation Group, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, North Carolina  2001-2005.
• Visiting Research Fellow, Calcium Regulation Group, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, North Carolina  2006-2007.
• Assistant Professor, Department of Physiology & Pharmacology, University of Toledo College of Medicine, HSC, Toledo, OH.  2007-2013. 
• Associate Professor, Department of Physiology & Pharmacology, University of Toledo College of Medicine, HSC, Toledo, OH.  2013-

Research interests:

Research in Dr. Vazquez’s lab is focused on the role of non-selective cation channels, such as Transient Receptor Potential Canonical (TRPC) channels and nicotinic acetylcholine receptors, in molecular and cellular events of atherosclerosis. Atherosclerosis is a disease of the arterial wall with a dominant and maladaptive inflammatory response, and represents the leading cause of death in western societies, remaining as the main vascular complication of metabolic diseases such as diabetes, obesity and metabolic syndrome. Our group has recently discovered that endothelial TRPC3 channels are an obligatory component of the signaling underlying regulated expression of cell adhesion molecules and macrophage recruitment to endothelium, two critical events throughout all stages of atherosclerotic lesion development. We have also discovered a novel nicotinic acetylcholine receptor-dependent survival pathway in coronary endothelium. More recently, our lab has shown that TRPC3, through a mechanism not yet defined, is critical for macrophage survival and efferocytosis. To study this, our lab makes use of in vitro (primary and immortalized cell lines) and in vivo (global and conditional transgenic and knockout mice; bone marrow transplantation) models of endothelial and macrophage dysfunction, and a number of techniques (including patch-clamp electrophysiology, real-time camera-based fluorescence imaging, real-time amperometry, protein chemistry/molecular biology, morphometric and immunohistochemical analysis of atherosclerotic lesions in mice).

Selected Publications:

Vazquez G, Lievremont JP, Bird GSJ, Putney J W. Jr. 2001. Human Trp3 forms both inositol trisphosphate receptor-dependent and receptor-independent store-operated cation channels in DT40 avian B lymphocytes. Proc. Natl. Acad. Sci. USA, 98, 11777-11782 PMID: 11553786

Vazquez G, Wedel B, Trebak M, Bird GSJ, Putney JW Jr. 2003. Expression Level of TRPC3 Channel Determines Its Mechanism of Activation. J.Biol.Chem., 278, 21649-21654 PMID: 12686562

Wedel B, Vazquez G, McKay R, Bird GSJ, Putney J W. Jr. 2003. A Calmodulin/IP₃ receptor binding region targets TRPC3 to the plasma membrane in a calmodulin/IP₃ receptor-independent process. J.Biol.Chem., 278, 25758-25765 PMID: 12730194

Trebak M, Vazquez G, Bird GSJ, Putney J W. Jr. 2003. The TRPC3/6/7 subfamily of cation channels. Cell Calcium, 33, 451-461 PMID: 12765690

Vazquez G, Wedel B, Aziz O, Trebak M, Putney JW Jr. 2004. The mammalian TRPC cation channels. Biochim.Biophys.Acta, 1742, 21-36 PMID: 15590053

Vazquez G, Wedel B, Kawasaki B, Bird GSJ, Putney JW Jr. 2004. Obligatory role of Src kinase in the signaling mechanism for TRPC3 cation channels. J.Biol.Chem., 279, 40521-40528 PMID: 15271991

Lievremont JP^§, Numaga^§ T, Vazquez G^§, Lemonnier L, Hara Y, Mori E, Trebak M, Moss S, Bird GSJ, Mori Y, Putney JW Jr. 2005. The role of Canonical Transient Receptor Potential 7 (TRPC7) in B-cell receptor-activated channels. J.Biol.Chem., 279, 40521-40528 (^§equally contributing authors). PMID: 16123040

Vazquez G, Bird GSJ, Mori Y, Putney JW Jr. 2006. Native Canonical Transient Receptor Potential 7 channel activation by an inositol trisphosphate receptor-dependent mechanism. J.Biol.Chem., 281,25250-25258. PMID: 16822861

Smyth TS, Lemonnier L, Vazquez G, Bird GSJ, Putney JW Jr. 2006. Dissociation of regulated trafficking of TRPC3 channels to the plasma membrane from their activation by phospholipase C. J.Biol.Chem., 281, 11712-11720 PMID: 16522635

Smedlund K, Vazquez G. 2008. Involvement of Native TRPC3 Proteins in ATP-dependent expression of VCAM-1 and Monocyte Adherence in Coronary Artery Endothelial Cells. Arterioscler, Thromb. Vasc. Biol., 28, 2049-2055. PMID: 18787184

Tano JY, Smedlund K, Vazquez G. 2010. Endothelial TRPC3/6/7 Proteins at the Edge of Cardiovascular Disease. Cardiovasc. Hematol. Agents Med. Chem. 8, 1-11. PMID: 20214601

Smedlund K, Tano JY, Vazquez G. 2010. The Constitutive Function of Native TRPC3 Channels Modulates VCAM-1 Expression in Coronary Endothelial Cells through NFkappaB Signaling. Circ Res 106, 1479-1488. PMID: 20360250

Vazquez G., Tano JY., Smedlund K. 2010. On the potential role of source and species of diacylglycerol in phospholipase-dependent regulation of TRPC3 channels. Channels (Austin) 4, 232-240 PMID: 20458187

Tano JY, Vazquez G. 2011. Requirement for non-regulated, constitutive calcium influx in macrophage survival signaling. Biochem. Biophys. Res. Commun., 407, 432-437. PMID: 21414290

Smedlund K, Tano JY, Margiotta J, Vazquez G. 2011. Evidence for operation of nicotinic and muscarinic acetylcholine receptor-dependent survival pathways in human coronary artery endothelial cells. J. Cell Biochem. May 3. doi: 10.1002/jcb.23169. [Epub ahead of print] PMID: 21541985

Vazquez G, Smedlund K, Tano JY, Lee R. 2011. Molecular and cellular aspects of atherosclerosis: emerging roles of TRPC channels. In: Coronary Artery Diseases, Ed: Angelo Squeri, MD InTech Publisher. ISBN 978-953-307-712-3.

Tano JY, Smedlund K, Lee R, Abramowitz J, Birnbaumer L, Vazquez G. 2011. Impairment of survival signaling and efferocytosis in TRPC3-deficient macrophages. Biochem. Biophys. Res. Commun., 410, 643-647. PMID: 21684255

Vazquez G. 2012. TRPC Channels as Prospective Targets in Atherosclerosis: terra incognita. Frontiers in Bioscience (Schol. Ed.), 4, 157-166. PMID: 22202050

Tano JY, Lee RH, Vazquez G.  2012. Involvement of calmodulin and calmodulin kinase II in tumor necrosis factor alpha-induced survival of bone marrow derived macrophages.  Biochemical and Biophysical Research Communications, 427, 178-184. PMID: 22989752

Smedlund K, Bah M, Vazquez G. 2012. On the role of endothelial TRPC3 channels in endothelial dysfunction and cardiovascular disease. Cardiovasc. Hematol. Agents Med. Chem. 10, 265-274. PMID:22827251              

Tano JY*, Lee RH*, Vazquez G. (*equally contributing authors) 2012. Macrophage function in atherosclerosis: potential roles of TRP channels. Channels (Austin), 6, 141-148. PMID: 22909953

Najjar SM, Ledford KJ, Abdallah S, Paus A, Russo L, Kaw M, Ramakrishnan S, Muturi HT, Raphael CK, Ghosh-Lester S, Heinrich G, Pierre SV, Benndorf R, Kleff V, Jaffa A, Lévy A, Vazquez G, Goldberg I, Beauchemin N, Scalia R, Ergün S.  2013. Ceacam1 null celetion causes vascular alterations in large vessels” American Journal of Physiology–Endocrinology and Metabolism, in press.