Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differential vulnerability of the major components of microtubules was examined in ischemic gerbil brains by a light microscopic, immunohistochemical method using monoclonal antibodies for microtubule-associated protein (MAP) 1A and MAP2, polyclonal antibody for MAP1 and 2 as well as monoclonal antibody for alpha-tubulin. Progressive cerebral ischemia during unilateral carotid occlusion for 5, 15 and 120 min and reperfusion for 3, 12 and 48 h following bilateral carotid occlusion for 10 min were studied. Ischemic lesions in the subiculum-CA1 region were visualized by all antibodies after ischemia for 5 min but the antibody for alpha-tubulin was less sensitive. The antibody for alpha-tubulin was also less sensitive than antibodies for MAPs for detection of early postischemic lesions. Differential sensitivity was also observed in the cerebral cortex and other brain regions. Microtubules in myelinated axons were more stable than those in dendrites. The observed loss of immunohistochemical reactivities for MAPs and alpha-tubulin may have been caused by activation of calcium-dependent proteolytic enzymes such as calpains. The discrepancy between MAPs and alpha-tubulin could be due to differences in affinities or topographic distributions of these proteins within microtubules.
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PMID:Differential vulnerability of microtubule components in cerebral ischemia. 225 7

Degradation of neurofilament (NF) triplet proteins (Mw 200,000 (NF200), Mw 150,000 (NF150), Mw 68,000 (NF68], high molecular weight microtubule-associated proteins (MAP1 and MAP2) and other cytoskeletal proteins in rat brain during ischemia was investigated by sodium dodecyl sulfate (SDS)-gel electrophoresis and immunoblot methods using anti-NF200 monoclonal antibody. Selective degradation of NF200 and NF150 was observed during the initial 10 to 15 minutes of ischemia: and the degradation of MAP1 and MAP2 during the initial 15 to 30 minutes of ischemia. These degradations suggest that the activation of a protease occurs at the very early stage of cerebral ischemia, which are the earliest irreversible neuronal changes ever to be reported. Effect of ischemia on polymerization of microtubule proteins was also investigated by turbidity assay. A rapid decrease of the ability of polymerizing microtubules was observed during the initial 5 minutes of ischemia. This loss of polymerization ability was apparently independent of the degradation of MAP1 and MAP2.
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PMID:[Degradation of cytoskeletal proteins in cerebral ischemia]. 280 16