Abstract

Brain edema (cytotoxic and vasogenic edema) and secondary brain injury are the major responses of the central nervous system to heterogenous primary pathological disorders including ischemia, trauma and hypoxia. The fundamental mechanisms of the edema development and neuronal injury following ischemia and trauma are major subjects of this research proposal. We will focus primarily on glutamate receptor (NMDA and non-NMDA), second messenger system (arachidonic acid, 1,4,5-inositol triphosphate), injury markers (heat shock proteins) and factors (oxygen radicals) that are associated with cellular swelling, membrane injury and cell death following cerebral ischemia and hypoxia. The factors generated by trauma and hypoxia that increase blood-brain barrier permeability and the subsequent development of vasogenic edema will be fully investigated. Thus the research projects of the CNS Injury and Edema Center provide for interdisciplinary studies ranging from the biochemical, physiological, and ultrastructural basis of various types of brain edema and neuronal injury to pharmacological manipulations.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Specialized Center (P50)
Project #
5P50NS014543-16
Application #
3107685
Study Section
Special Emphasis Panel (SRC (03))
Project Start
1991-09-01
Project End
1996-06-30
Budget Start
1993-08-24
Budget End
1994-06-30
Support Year
16
Fiscal Year
1993
Total Cost
Indirect Cost

  Institution

Name
University of California San Francisco
Department
Type
Schools of Medicine
DUNS #
073133571
City
San Francisco
State
CA
Country
United States
Zip Code
94143

  Publications

Kim, Jong Youl; Kim, Nuri; Yenari, Midori A et al. (2013) Hypothermia and pharmacological regimens that prevent overexpression and overactivity of the extracellular calcium-sensing receptor protect neurons against traumatic brain injury. J Neurotrauma 30:1170-6
Voloboueva, Ludmila A; Emery, John F; Sun, Xiaoyun et al. (2013) Inflammatory response of microglial BV-2 cells includes a glycolytic shift and is modulated by mitochondrial glucose-regulated protein 75/mortalin. FEBS Lett 587:756-62
Sakata, Hiroyuki; Niizuma, Kuniyasu; Wakai, Takuma et al. (2012) Neural stem cells genetically modified to overexpress cu/zn-superoxide dismutase enhance amelioration of ischemic stroke in mice. Stroke 43:2423-9
Tang, Xian Nan; Cairns, Belinda; Kim, Jong Youl et al. (2012) NADPH oxidase in stroke and cerebrovascular disease. Neurol Res 34:338-45
Cairns, Belinda; Kim, Jong Youl; Tang, Xian Nan et al. (2012) NOX inhibitors as a therapeutic strategy for stroke and neurodegenerative disease. Curr Drug Targets 13:199-206
Voloboueva, Ludmila A; Giffard, Rona G (2011) Inflammation, mitochondria, and the inhibition of adult neurogenesis. J Neurosci Res 89:1989-96
Tang, Xian N; Zheng, Zhen; Giffard, Rona G et al. (2011) Significance of marrow-derived nicotinamide adenine dinucleotide phosphate oxidase in experimental ischemic stroke. Ann Neurol 70:606-15
Chen, Hai; Kim, Gab Seok; Okami, Nobuya et al. (2011) NADPH oxidase is involved in post-ischemic brain inflammation. Neurobiol Dis 42:341-8
Yoshioka, Hideyuki; Niizuma, Kuniyasu; Katsu, Masataka et al. (2011) NADPH oxidase mediates striatal neuronal injury after transient global cerebral ischemia. J Cereb Blood Flow Metab 31:868-80
Xiong, Xiaoxing; Barreto, George E; Xu, Lijun et al. (2011) Increased brain injury and worsened neurological outcome in interleukin-4 knockout mice after transient focal cerebral ischemia. Stroke 42:2026-32

Showing the most recent 10 out of 103 publications