Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immunoreactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.
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PMID:An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia. 172 31

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

Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic microtubule-associated protein, MAP2, may occur after short periods of transient global ischemia. tau, a predominantly axonal microtubule-associated protein, has not been examined following ischemia. We compared neuronal damage with alterations in MAP2, tau, and 72-kD heat shock protein (HSP72) immunostaining at various reperfusion times following 20 min of ischemia in the rat four-vessel occlusion model. tau accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikaryal tau immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immunostaining in the target of many hilar neurons, the inner molecular layer of the dentate gyrus. The same neuronal populations that exhibited increased tau immunostaining of perikarya later displayed an induction of HSP72 immunoreactivity. In contrast, loss of MAP2 immunostaining was not consistently observed before neuronal death and did not correspond to HSP72 induction. The altered tau immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of tau, but did cause disruption of MAP2 immunostaining. Taken together, the results suggest that the somal accumulation of tau is an early, sensitive, and selective marker of ischemic insult.
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PMID:Alterations in tau immunostaining in the rat hippocampus following transient cerebral ischemia. 751 35

Sequential changes of [3H]glycine binding in the gerbil were investigated in selectively vulnerable areas 1 h to 7 days after 10 min of cerebral ischemia. A significant reduction in [3H]glycine binding was found in the hippocampus and thalamus from as early as 1 h after ischemia. In contrast, the striatum and frontal cortex showed a significant decline in [3H]glycine binding from 5 h after recirculation. Thereafter, a severe reduction in [3H]glycine binding was observed in all regions 7 days after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity was unaffected in the hippocampus, frontal cortex and thalamus up to 48 h after ischemia. Thereafter, a severe loss of MAP2-immunoreactive neurons was found in these regions, especially in the hippocampal CA1 sector. However, the striatum showed a severe loss of MAP2 immunoreactivity from 24 h after ischemia. These results demonstrate that transient cerebral ischemia causes severe reduction in [3H]glycine binding throughout the brain, and this reduction precedes the neuronal damage in selectively vulnerable areas. These findings suggest that a neurotransmitter, glycine, may play a key role in the pathogenesis of post-ischemic neurodegeneration in selectively vulnerable areas.
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PMID:Post-ischemic changes of [3H]glycine binding in the gerbil brain after cerebral ischemia. 767 5

Changes of immunoreactivities for microtubule based motor proteins, kinesin and cytoplasmic dynein, and non-motor protein, microtubule associated protein (MAP) 2 were investigated in gerbil hippocampus after transient ischemia. The immunoreactivities for kinesin showed a progressive decrease in hippocampal CA1 cells from 8 h after transient 5 or 15 min of ischemia that is lethal to the CA1 cells, while it showed no change after 2 min of ischemia that is non-lethal to the cells. The immunoreactivities for cytoplasmic dynein showed a decrease from 3 or 1 h of reperfusion in the CA1 cells after 5 or 15 min of ischemia, respectively. In contrast, the immunoreactivity for MAP2 remained normal until 2 days in the CA1 cells after 5 min of ischemia. These results showed an early changes of microtubule based motor proteins, such as kinesin and cytoplasmic dynein in vulnerable CA1 neurons. These changes may affect the mitochondrial shuttle system between neuronal cell body and the peripheries such as axon terminal and dendrites. This early disturbance may cause a failure to obtain newly synthesized nuclear encoded mitochondrial protein, and result in mitochondrial dysfunctions and the subsequent cell death.
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PMID:Early immunohistochemical changes of microtubule based motor proteins in gerbil hippocampus after transient ischemia. 771 74

Immunohistochemical changes of striatal interneurons in the gerbil were investigated 1 h-7 days after 10 min cerebral ischemia. Marked reduction of parvalbumin-immunoreactive interneurons was seen in the striatum from 24 h after ischemia. MAP2 (microtubule-associated protein 2) immunoreactivity markedly decreased in striatal neurons 5 h after ischemia but was unaffected in interneurons. Thereafter, a severe loss of MAP2 immunoreactivity in the interneurons was found 48 h and 7 days after ischemia. The results demonstrate that transient cerebral ischemia can cause a loss of parvalbumin and MAP2 immunoreactivity in interneurons in the dorsolateral striatum in a delayed fashion as compared with a rapid loss of striatal neurons.
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PMID:Delayed damage of striatal interneurons after cerebral ischemia in the gerbil. 797 Feb 28

The effect of naftidrofuryl, a drug used in ischemia for its vasodilator properties and its protective effect on neuronal survival, was investigated on the maturation of cultured chicken spinal cord neurons, focusing on the presence of proteins specific for the developing neuronal cytoskeleton. Although no influence of naftidrofuryl on the rate of growth of neurites was observed, the drug enhanced the relative amount of the high molecular weight neurofilament subunit without affecting the concentration of a microtubule-associated protein, MAP2. These findings suggest that the effect of naftidrofuryl on cultured spinal cord neurons might involve molecular events directly associated with the induction of a mature cytoskeleton architecture, instead of stimulating undifferentiated neurite growth.
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PMID:Naftidrofuryl, a putative activator of neuron survival, stimulates the expression of neurofilament heavy subunit in cultivated spinal cord neurons from chicken. 816 24

Post-ischemic treatment of di-Calciphor (16,16'-dimethyl-15- dehydroprostaglandin B1) significantly improves animal survival and prevents ischemia-induced neurodegeneration of vulnerable forebrain regions assessed with histochemical and biochemical techniques in gerbils. Neuronal degeneration seen by Cresyl violet staining and silver impregnation in the CA1 sector of the hippocampus and the dorso-lateral sector of the striatum was significantly reduced in animals treated with di-Calciphor. In addition, the early onset of selective degradation of calpain I substrates spectrin and microtubule-associated protein (MAP2) in these same vulnerable regions was prevented. The lack of adverse side effects may facilitate the potential therapeutic use of this drug in preventing neuronal damage caused by stroke.
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PMID:Neuroprotective activity of dimer of 16,16'-dimethyl-15-dehydroprostaglandin B1 (di-Calciphor) in cerebral ischemia. 846 94

Changes in drebrin, MAP2 (postsynaptic marker) and synaptophysin (presynaptic marker) in rat brains were examined after 20 min of transient cerebral ischemia. Immunoreactivity for drebrin and MAP2 in hippocampus CA1 area decreased 7 days after ischemia. The immunoreactivity for debrin in stratum lucidum of hippocampus CA3 area increased 7 days after ischemia. Sodium dodecyl sulfate gel electrophoresis and immunoblot procedures using an antibody to drebrin, MAP2 and synaptophysin were carried out. The levels of drebrin and MAP2 in hippocampus decreased significantly 4 hours and 7 days after recirculation. In contrast, the level of synaptophysin was unchanged. The levels of each protein in cerebral cortex showed no significant changes. The changes after ischemia seemed to occur at the same time both in the dendritic spines and in their shafts, and the increase of the immunoreactivity for drebrin in CA3 might suggest the change of cytoskeletal protein synthesis in survived neurons.
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PMID:[The changes of central nervous synapses after transient cerebral ischemia]. 858 59


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