Portrait - Linda Cai

   Dr. H. Linda Cai, MD, PhD
   Professor of Anesthesiology and
   Medicine/Cardiology (tenured)
   Cardiovascular Research
   Laboratories Principal Investigator
   Cai Laboratory

   Email: hcai@mednet.ucla.edu
   Phone: (310) 267-2303
   Fax: (310) 825-0132

   UCLA
   David Geffen School of Medicine
   Department of Anesthesiology
   Division of Molecular Medicine
   650 Charles E Young Dr.
   BOX 957115, BH - 550 CHS
   Los Angeles, CA 90095-7115
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Welcome to the homepage of the Cai Laboratory! We belong to the Division of Molecular Medicine, Department of Anesthesiology. We are also part of the Cardiovascular Research Laboratories and Department of Medicine, Division of Cardiology. As the Principle Investigator of the group, I appreciate you visiting our webpage and hope that you find our research exciting.

We are interested in reactive oxygen species regulation of endothelial nitric oxide synthase (eNOS) expression and function, and its consequences regarding nitric oxide bioavailability and development of cardiovascular diseases. Nitric oxide is an important signaling molecule. It relaxes vascular smooth muscle to dilate blood vessels. It also inhibits a variety of pathological events such as activation of platelets and induction of inflammatory proteins. Loss of nitric oxide leads to high blood pressure and atherosclerotic vascular diseases. It is of great clinical significance to fully understand regulation of nitric oxide bioavailability at molecular levels.

Data accumulated in the past decade have shown that production of reactive oxygen species is increased in aging, cardiovascular and pulmonary diseases, neurodegenerative disorders and angiogenesis. An important consequence of excessive production of reactive oxygen species is oxidative inactivation of nitric oxide. For example, superoxide radicals rapidly react with nitric oxide to form peroxynitrite, resulting in immediate loss of nitric oxide. Additional recent studies suggest that reactive oxygen species can oxidize tetrahydrobiopterin, an essential cofactor for eNOS. This response leads to a condition where eNOS produces superoxide rather than nitric oxide. This "uncoupling" phenomenon of eNOS likely prolongs oxidative stress. Our goal is to characterize in-depth molecular mechanisms whereby eNOS uncouples under disease states. This will ultimately lead to discovery of novel therapeutics restoring nitric oxide production from uncoupled eNOS, in other words, "recoupling" of eNOS.

One focus in the lab is to explore molecular mechanisms and consequences of eNOS uncoupling in various forms of vascular diseases such as hypertension, abdominal aortic aneurysm, atherosclerosis, and diabetic vascular disease using a combination of molecular and cell biological, genetic and physiological approaches. We are also interested in defining nitric oxide-dependent innovative angiogenic pathways, oxidative mechanisms of ischemia reperfusion (I/R) induced cardiac injury and protection by a novel protein netrin-1, molecular mechanisms underlying the most common cardiac arrhythmia atrial fibrillation and its thromboembolic complications, and a causal role of vascular oxidative stress of development of obesity and metabolic syndrome.

Current Research Projects

Copyright 2007