Guillermo Vazquez, Ph.D.
Associate Professor, Department of Physiology and Pharmacology
Director, Vascular Physiology Program
Associate Director, Center for Hypertension and Personalized Medicine
Phone: (419) 383-5301
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
- Member of the International Advisory Committee on Science, Argentinean Ministry of Science and Technology, Argentina 2016- present.
- 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-present.
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).
Please see a complete list of Dr. Vazquez's publications here.