Rona Giffard

Administrative Appointments

• Vice-Chair for Research, Dept. of Anesthesia (1999 - present)

Honors and Awards

• NIH Clinical Investigator Award, NIH (1990-1995)
• Young Investigator Award, Foundation for Anesthesia Education and Research (1991-1992)
• Ellen Weaver Award, Association for Women in Science, Northern California Chapters (1997)
• Frontiers in Anesthesia Research Award, International Anesthesia Research Society (1998-2003)
• AHA/Bugher Award, American Heart Association (2000-2004)

Professional Education

Postdoctoral Advisees

George Barreto, Yajing Hu, Ludmila Voloboueva, Xiaoxing Xiong

Graduate & Fellowship Program Affiliations

• Anesthesia
• Neurosciences
• Neurosurgery
• Neonatology and Developmental Biology
• Cell Biology
• Molecular and Genetic Medicine

Web Site Links

• Giffard Lab Web site

Research Interests

Brain injury from stroke, head trauma, and chronic neurologic degenerative diseases, is a major cause of morbidity and mortality. We are particularly interested in the cellular consequences of brain injury. To study this problem we work with primary cultures of neurons and astrocytes from mice in addition to employing rodent models of stroke. Current work focuses on: 1) the role of astrocytes in brain injury; 2) the interaction of neurons and glia during injury; 3) protection using heat shock protein and anti-apoptotic protein overexpression 4) changes in mitochondrial function and signaling in injury; 5) the interaction of oxidative stress and inflammation in stroke; 6) computational modeling of cell death.
We use gene transfer techniques to express genes of interest in brain cells and intact brain and analyze ways in which these genes can provide protection. We use fluorescent probes for pH, intracellular calcium, ROS, mitochondrial membrane potential, glutathione, as well as morphologically evaluate outcome, and quantitate injury. We also use transgenic mice to analyze the effects of overexpression or loss of expression of specific genes on outcome from stroke. Mitochondria are central to both energy metabolism and the regulation of cell death. We study changes in mitochondria with stress. We are also interested in the interaction of oxidative stress and inflammation in stroke.

A new area for us is computational modeling of cell death and the effects of heat shock proteins. We are working on an ODE control model.

Publications

• Postischemic brain injury is attenuated in mice lacking the beta2-adrenergic receptor. Han RQ, Ouyang YB, Xu L, Agrawal R, Patterson AJ, Giffard RG. Anesth Analg. 2009; 108 (1): 280-7
• Inflammation and NFkappaB activation is decreased by hypothermia following global cerebral ischemia. Webster CM, Kelly S, Koike MA, Chock VY, Giffard RG, Yenari MA. Neurobiol Dis. 2009; 33 (2): 301-12
• Overexpression of mitochondrial Hsp70/Hsp75 in rat brain protects mitochondria, reduces oxidative stress, and protects from focal ischemia. Xu L, Voloboueva LA, Ouyang Y, Emery JF, Giffard RG. J Cereb Blood Flow Metab. 2009; 29 (2): 365-74
• Overexpression of mitochondrial Hsp70/Hsp75 protects astrocytes against ischemic injury in vitro. Voloboueva LA, Duan M, Ouyang Y, Emery JF, Stoy C, Giffard RG. J Cereb Blood Flow Metab. 2008; 28 (5): 1009-16
• Regulation of apoptotic and inflammatory cell signaling in cerebral ischemia: the complex roles of heat shock protein 70. Giffard RG, Han RQ, Emery JF, Duan M, Pittet JF. Anesthesiology. 2008; 109 (2): 339-48