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)

We tested the hypothesis that populations of ependymal, subependymal and choroid plexus cells proliferate and differentiate after stroke in adult rats. Rats were subjected to 2 h of middle cerebral artery occlusion (n=70) and euthanized at 1, 2, 4, 7, 14, 21 and 28 days (10 per time point). Hematoxylin and eosin staining and immunostaining were performed using antibodies against bromodeoxyuridine, neuronal nuclear antigen and glial fibrillary acidic protein after stroke. In normal nonischemic rats (n=10), single layers of ependymal and choroid plexus cells do not react with bromodeoxyuridine, neuronal nuclear antigen or glial fibrillary acidic protein. Individual subependymal cells express glial fibrillary acidic protein and bromodeoxyuridine, but not neuronal nuclear antigen. After stroke, increased bromodeoxyuridine reactivity was present in multiple layers of ependymal cells and nodules of subependymal cells and in scattered choroid plexus cells from 2 to 28 days and peaked at 7 days. Bromodeoxyuridine immunoreactivity colocalized with neural phenotypes of neuronal nuclear antigen (approximately 0.1-3.5%) and glial fibrillary acidic protein (approximately 8.6%) immunoreactivity in cells in the ventricular zone and the subventricular zone, as well as in the choroid plexus of the ischemia affected hemisphere. Our data suggest that ependymal, subependymal and choroid plexus cells are potential neural precursor cells in the adult mammalian brain.
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PMID:Cell proliferation and differentiation from ependymal, subependymal and choroid plexus cells in response to stroke in rats. 1179 Mar 94

Many factors contribute to the severity of neuronal cell death and the functional outcome in stroke. We describe an embolic model of focal cerebral ischemia in the rat that does not require craniotomy and is compatible with continuous measurement of regional CBF using multichannel laser Doppler flow (LDF) technique. Either a 22 microliters (large lesion) or 11 microliters (small lesion) bolus of viscous silicone was injected cephalad into the internal carotid artery. Upon injection, LDF decreased abruptly, most severely in the parietal cortex (-74% +/- 5%) in the large lesion and in the occipital cortex (-69% +/- 10%) in the small lesion model. Over the first hour, post-embolization LDF improved in most areas (e.g. -48% +/- 9% parietal, large lesion) but declined in the small lesion group in the occipital region (-81% +/- 8%). CBF measured by [C]14-IAP autoradiography 1 h post-embolization in the large lesion model demonstrated near-hemispheric ischemia (70% of hemisphere) with sparing of cingulate cortex. Autoradiography demonstrated that ischemia in the small lesion was largely cortical. Light microscopy of brains embolized with 11 microliters of dyed silicone showed filling of pial vessels with no silicone in the Circle of Willis or parenchyma. No animals in the large lesion group survived 24 h. Thirteen of 15 animals in the small lesion group survived for two weeks with resolution of initial hemiplegia, ocular asymmetry and weight loss. Hematoxylin-eosin staining two weeks post-embolization showed signs of severe hypoxia and infarction. In conclusion, the intracarotid silicone embolization technique produces a titrable, reproducible permanent ischemic injury by blocking perfusion in the pial circulation, and is amenable to multisite monitoring with laser Doppler flowmetry. The smaller embolus produces cortical infarction with high rate of survival and neurological recovery.
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PMID:Focal cerebral ischemia in rats produced by intracarotid embolization with viscous silicone. 1187 3

We studied the expression of brain-derived neurotrophic factor (BDNF) immunoreactivity and mRNA in the ischemia-vulnerable cerebral hippocampal CA1 and cortical areas after permanent occlusion of bilateral internal carotid arteries. Four groups of rats were studied, including 1) young normotensive Wistar-Kyoto (WKY) rats, 2) aged normotensive WKY rats, 3) young spontaneous hypertensive rats (SHR), and 4) aged SHR. Each group contained rats from sham operation and 1 week, 4 weeks, and 8 weeks after cerebral ischemia (n = 3-5 at each time point). Hematoxylin and eosin staining and in situ apoptosis detection showed no neuronal damage from 1 week to 8 weeks in all the ischemic rats. Immunohistochemistry and Western blot showed that BDNF immunoreactivity increased only at 1 week in the CA1 area of young WKY rats (P < .001) and SHR (P = .002) and decreased only at 8 weeks in the cortical area of aged WKY rats (P = .02). In situ hybridization and TaqMan real-time RT-PCR showed that BDNF mRNA decreased consistently from 1 week to 8 weeks in both CA1 and cortical areas in young SHR (P < .05 and P < .01, respectively) and in aged WKY rats (P < .01 and P < .05, respectively) but was not changed in young WKY rats or aged SHR (P > .05) compared with the sham-operated rats. Our study demonstrates an expression disparity of BDNF immunoreactivity and mRNA in the hippocampal CA1 and cortical areas, especially in the young SHR and aged WKY rats after mild cerebral ischemia. Our study suggests that, under permanent occlusion of bilateral internal carotid arteries, aging and the level of blood pressure may have influence on the expression of BDNF.
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PMID:Expression of brain-derived neurotrophic factor immunoreactivity and mRNA in the hippocampal CA1 and cortical areas after chronic ischemia in rats. 1513 29

NeuN immunoreactivity is used as a specific marker for neurons. The number of NeuN-positive cells decreases under pathological conditions. This finding is usually considered as an evidence of neuronal loss. However, decrease in NeuN labeling may also be caused by depletion of the protein or loss of its antigenicity. Hence, we have investigated the morphological features of neurons that lost NeuN immunoreactivity and the NeuN protein levels in mouse brain after cerebral ischemia. The number of NeuN-labeled cells was decreased 6 h after a mild ischemic insult (30 min middle cerebral artery occlusion) in penumbral and core regions. Hematoxylin and eosin (H&E) staining of adjacent sections showed that neurons in the penumbra were not disintegrated but displayed early ischemic changes. The nuclear NeuN staining was dramatically reduced or lost in some neurons. However, Hoechst 33258 staining of the same sections revealed that these nuclei were preserved with an intact membrane. Labeling of neurons that had lost NeuN-positivity with antibodies against caspase-3-p20, which is constitutively not present but emerges in neurons after ischemia, disclosed that these neurons still preserved their integrity. Moreover, Western blots showed that NeuN protein levels were not decreased, suggesting that reduced NeuN antigenicity accounted for loss of immunoreactivity in this mild brain injury model. Supporting this idea, NeuN labeling was partially restored after antigenic retrieval. In conclusion, since NeuN immunoreactivity readily decreases after metabolic perturbations, reduced NeuN labeling should not be taken as an indicator of neuronal loss and, quantitative analysis based on NeuN-positivity should be used cautiously after central nervous system (CNS) injury.
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PMID:Loss of NeuN immunoreactivity after cerebral ischemia does not indicate neuronal cell loss: a cautionary note. 1522 81

There is a demand for studying the role of Toxoplasma gondii in cell death seeking aiding prevention of the disease. The neuro-pathological changes in the cerebellum cortex in case of acquired toxoplasmosis had been studied. Adult Balb C mice were infected by intra peritoneal injection of T. gondii RH strain. Immuno-histochemical expression of pro apoptotic marker Bax had been applied in parallel with Hematoxylin and Eosin stain to study the layers of cerebellum cortex. The focal necrosis in the cerebellum was expressed. Necrosis was explained on the basis of hypoxic ischemia resulting from existing vasculitis followed the infection. Purkinje cell layer was markedly affected in the form of disfiguring and focal loss of cells with apoptotic and necrotic changes. Thinning of both the molecular and internal granular layers was recorded morphometricly. Morphometric study reveals non significant change in the ratio between the viable to non viable cells in all cerebellum layers among experimental and control groups though the Purkinje cell layer was mostly affected. Statistical significant changes in depth proportion of molecular layer: Internal granular (ML: IGL) layers was noted in experimental and control group (p=0.05). Bax expression was not coexisting with the result of H & E stained cells. The hypothesis emphasizes that toxoplasmosis resist apoptosis seeking its benefit, and apoptosis followed toxoplasmosis may be due to another protein rather than Bax.
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PMID:Cell death pattern in cerebellum neurons infected with Toxoplasma gondii. 1633 90

We studied the effect of hypertension on brain damage and brain-derived neurotrophic factor (BDNF) expression in the hippocampal formation and cerebral cortex after permanent occlusion of bilateral common carotid arteries (CCA). Two groups of rats were used, including normotensive Wistar-Kyoto (WKY) rat and spontaneous hypertensive rat (SHR). Each group contained sham operation, 1 week and 4 weeks after bilateral CCA occlusion (n=5-10 in each time point). The blood pressure showed a significant elevation in WKY rats from 1 h after operation to 4 weeks before sacrifice (P<0.05), but was not changed in SHR (P>0.05). However, rectal temperature showed no significant change after operation in WKY rat and SHR (P>0.05) and showed no significant difference at any time point between WKY rat and SHR (P>0.05). Hematoxylin and eosin staining showed SHR had a significantly larger necrotic volume than WKY rats (n=10 in each group, 6044+/-6895 microm(3) vs. 144+/-174 microm(3), P<0.05) at 4 weeks after ischemia. In SHR, BDNF immunoreactivity and mRNA decreased significantly from 1 week to 4 weeks in both the hippocampal CA1 and cortical areas (P<0.01) but decreased transiently in dentate gyrus. However, in WKY rats, BDNF immunoreactivity and mRNA decreased transiently at 1 week (P<0.05) and recovered at 4 weeks after cerebral ischemia. Our study demonstrates that after bilateral CCA occlusion, preexisting hypertension may aggravate the brain injury and downregulate the expression of BDNF immunoreactivity and mRNA in the ischemia-vulnerable hippocampal CA1 and cortical areas but not in ischemia-resistant dentate gyrus.
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PMID:Hypertension downregulates the expression of brain-derived neurotrophic factor in the ischemia-vulnerable hippocampal CA1 and cortical areas after carotid artery occlusion. 1696 81

It has been indicated that Src family protein tyrosine kinases (SrcPTKs) potentiate N-methyl-D-aspartate (NMDA) receptor function by phosphorylating NR2A subunits and that postsynaptic density protein 95 (PSD-95) facilitates this regulation. In this paper, we define the role of SrcPTKs in delayed neuronal damage following transient brain ischemia and explore the underlying mechanisms involved in this event. Transient global brain ischemia was induced by the four-vessel occlusion method. A specific Src family kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyramidine) and a PP2 negative control PP3 (4-amino-7-phenylpyrazolo[3,4-d]pyramidine) were infused into rat cerebroventricule 30 min before occlusion. Hematoxylin and eosine staining showed that the number of surviving pyramidal neurons in rat hippocampal CA1 subfield increased markedly in PP2-treated rats comparing to PP3-treated groups after 5 days of reperfusion following ischemia. Additionally, immunoprecipitation and immunoblot analysis revealed that preadministration of PP2, but not PP3, attenuated not only the increased tyrosine phosphorylation of NR2A but also the enhanced interactions among Src, NR2A and PSD-95 induced by ischemia/reperfusion. In conclusion, SrcPTKs promote binding of the kinases and their substrate NR2A attributed to the scaffolding effect of PSD-95 during transient brain ischemia and reperfusion, which are responsible for the elevation of NR2A tyrosine phosphorylation and consequent delayed neuronal cell death.
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PMID:PP2, a potent inhibitor of Src family kinases, protects against hippocampal CA1 pyramidal cell death after transient global brain ischemia. 1755

Endonuclease G is a mitochondrial enzyme, known to be translocated to the nucleus after transient focal cerebral ischemia and contribute to DNA degradation. After global cerebral ischemia, delayed cell death is observed in the thalamic reticular nucleus but the mechanisms involved are not well described. The purpose of this study was to identify if Endonuclease G was expressed in the cell nucleus of parvalbumin(+) GABA'ergic neurons in relation to cell death after global cerebral ischemia in the thalamic reticular nucleus. The cell death in male Wister rats were studied from 6 h until 4 days after global cerebral ischemia induced by transient 2-vessel carotid occlusion with hypotension for 15 min. Hematoxylin-eosin staining and immunohistochemistry for Endonuclease G, Parvalbumin and Glial fibrillary acidic protein was performed after the ischemic insult. Eosinophilic neurons and vacuolization of the cytoplasm in parvalbumin(+) neurons were observed 2 days after ischemia. Endonuclease G immunoreactivity increased in the cytoplasm 12 h after ischemia and was translocated to the nucleus of parvalbumin(+) neurons after 24 h. In the nucleus of astroglia, Endonuclease G was expressed after 2 days with an apoptotic-like morphology and the number of Endonuclease G-expressing astroglia increased during the later time points. During the same period the number of parvalbumin(+) neurons decreased. In conclusion, this study has identified that Endonuclease G is translocated from the cytoplasm to the nucleus of neurons and expressed with apoptotic-like morphology in the nucleus of astroglia in the thalamic reticular nucleus after global cerebral ischemia.
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PMID:Endonuclease G expression in thalamic reticular nucleus after global cerebral ischemia. 1856 42

The aim of this study was to examine the effect of iloprost in renal injury induced by abdominal aortic ischemia-reperfusion (IR) and how it can modulate the expression of adhesion molecules during this effect. Twenty-four Wistar-Albino rats were randomized into three groups (n=8) as follows: control (sham laparotomy), aortic IR (120 min ischemia and 120 min reperfusion), and aortic IR + iloprost (0.45 microg/kg/hr intravenous infusion during 120 min reperfusion). Blood and renal tissue samples were obtained for biochemical analysis. A histological evaluation with both hematoxylin-eosin staining and immunostaining was also done. Biochemical analyses showed that aortic IR significantly increased (p<0.05 vs. control) whereas iloprost significantly decreased (p<0.05 vs. aortic IR) plasma levels of malondialdehyde, P-selectin, intercellular adhesion molecule-1 (ICAM-I), and tissue levels of malondialdehyde and catalase. Histological evaluation with immunostaining showed that aortic IR significantly increased (p<0.05 vs. control) whereas iloprost significantly decreased (p<0.05 vs. aortic IR) the immunoreactivity of P-selectin, tumor necrosis factor-alpha, CD11b, CD18, and ICAM-1. Hematoxylin-eosin staining showed that iloprost also attenuated the morphological changes associated with aortic IR. The results of this study show that iloprost reduces renal injury induced by aortic IR in rats and downregulates expression of adhesion molecules at both the local and systemic levels after aortic IR during this protective effect.
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PMID:Iloprost downregulates expression of adhesion molecules and reduces renal injury induced by abdominal aortic ischemia-reperfusion. 1877 89

Changes in carbohydrate metabolism in brain injury and the involvement of numerous glycoproteins in the subsequent restoration phenomena orientated this paper towards reporting on glucidic radical distribution in postinjured brain tissue. Samples from nine patients suffering severe head injuries and three matched controls were studied. Autopsies were performed up to 24 h postmortem; brains were fixed in formalin and samples were taken from contusional, pericontusional and different brain regions including the anterior cingulum and corpus callosum, parasagittal gyrus, putamen, hippocampus and opercular areas embedded in paraffin. Hematoxylin-eosin staining, immunoreaction with glial fibrillary acid protein (GFAP) and biotin-conjugated lectins (RCA, UEA, PNA, concanavalin A (Con A) and WGA) were used. Contusion and related phenomena such as ischemia induced changes in lectin expression in several elements of the nervous tissue. Endothelial cells of contused areas were positive for RCA, UEA and progressively for WGA and Con A, which could be related to hemorheological disturbances inducing secondary brain damage. Neurons in affected areas were also stained for Con A and UEA, with some processes being delineated. Axonal swellings showed particular affinity to any lectin. Reactive astrocytes displaying only mild staining to WGA in cell bodies were strongly positive for GFAP, showing different patterns of reactivity in the cortex and in white matter.
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PMID:Changes in glucidic radicals in contused human brains. 1951 44


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