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Unilateral Middle Cerebral Artery Occlusion (unilateral + middle_cerebral_artery_occlusion)
Selected AbstractsInvolvement of , protein kinase C in estrogen-induced neuroprotection against focal brain ischemia through G protein-coupled estrogen receptorJOURNAL OF NEUROCHEMISTRY, Issue 4 2005Shigeto Hayashi Abstract The neuroprotective effects of estrogen were studied in the ischemic model mice by 90 min transient unilateral middle cerebral artery occlusion (MCAO) followed by 22.5 h reperfusion. The total infarct size in C57BL/6 female mice after MCAO and reperfusion was significantly smaller than that in male mice. Intraperitoneal injection of estrogen after the start of reperfusion significantly reduced the infarct volume in the male mice. However, no significant gender difference was found in total infarct size in , protein kinase C (PKC)-knockout mice, suggesting that the neuroprotective effects of estrogen are due to the activation of a specific subtype of PKC, ,PKC, a neuron-specific PKC subtype, in the brain. We demonstrated that exogenous estrogen-induced neuroprotection was attenuated in ,PKC-knockout mice. Immunocytochemical study showed that ,PKC was translocated to nerve fiber-like structures when observed shortly after MCAO and reperfusion. We also visualized the rapid and reversible translocation of ,PKC-GFP (green fluorescent protein) by estrogen stimulation in living CHO-K1 cells. These results suggest that the activation of ,PKC through the G-protein-coupled estrogen receptors on the plasma membrane is involved in the estrogen-induced neuroprotection against focal brain ischemia. [source] Protective role of COMP-Ang1 in ischemic rat brainJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2010Hye Young Shin Abstract In cerebral ischemia, the induction of angiogenesis may represent a natural defense mechanism that enables the hypoxic brain to avoid progression into infarction. Angiopoietin-1 (Ang1) is known to produce non-leaky and stable blood vessel formation mainly by the Tie2 receptor. Therefore, we envisioned that the application of cartilage oligomeric matrix protein-Ang1 (COMP-Ang1), a soluble, stable, and potent form of Ang1, would promote angiogenesis and provide a protective effect following unilateral middle cerebral artery occlusion (MCAO) in rats. To this end, we employed a 2-hour-MCAO model, and treated rats with adenovirus encoding COMP-Ang1 (Ade-COMP-Ang1) or control virus encoding ,-gal (Ade-,-gal). Time course magnetic resonance images (MRIs) revealed significantly reduced infarct volume in the rats treated with Ade-COMP-Ang1 with an improvement of post-ischemic neurological deficits compared with rats treated with Ade-,-gal. Moreover, compared to the rats treated with Ade-,-gal, the rats treated with Ade-COMP-Ang1 showed an increase in blood vessels, especially in the border zone adjacent to the infarction, increased number of endogenous neuronal progenitor cells in the ischemic brain, and decreased number of TUNEL-positive cells. Taken together, COMP-Ang1 reduced infarct volume and consequently attenuated post-ischemic neurological deficits through enhanced angiogenesis and increased viable cell mass of neuronal cells. © 2009 Wiley-Liss, Inc. [source] Endogenous neurogenesis and neovascularization in the neocortex of the rat after focal cerebral ischemiaJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2008Hye Young Shin Abstract The present study was designed to examine whether endogenous neurogenesis and neovascularization occur in the neocortex of the ischemic rat brain after unilateral middle cerebral artery occlusion (MCAO). Sprague-Dawley rats were divided into six groups (n = 29): one control group (n = 4) and five groups composed of animals sacrificed at increasing times post-MCAO (2 days and 1, 2, 4, and 8 weeks; n = 5 per group). To determine the presence of neurogenesis and neovascularization in the ischemic brain, nestin, Tuj1, NeuN, GFAP, Tie2, RECA, and 5-bromo-2,-deoxyuridine (BrdU) were analyzed immunohistochemically. In addition, nestin, GFAP, and Tie2 expression was determined by Western blotting. Triple-labeling of nestin, BrdU, and laminin was performed to visualize the interaction between endogenous neurogenesis and neovascularization. The number of BrdU- and nestin-colabeled cells increased markedly in the neocortex and border zone of the ischemic area up to 1 week after MCAO and decreased thereafter. Western blot analysis revealed that the expression of nestin, Tie-2, and GFAP was amplified in the ipsilateral hemisphere 2days after MCAO and peaked 1 week after MCAO, compared with that in the normal brain. After ischemic injury, nestin- and BrdU-colabeled cells were observed in the vicinity of the endothelial cells lining cerebral vessels in the ipsilateral neocortex of the ischemic brain. Endogenous neurogenesis and neovascularization were substantially activated and occurred in close proximity to one other in the ipsilateral neocortex of the ischemic rat brain. © 2007 Wiley-Liss, Inc. [source] Proton transfer ratio, lactate, and intracellular pH in acute cerebral ischemiaMAGNETIC RESONANCE IN MEDICINE, Issue 4 2007Kimmo T. Jokivarsi Abstract The amide proton transfer ratio (APTR) from the asymmetry of the Z -spectrum was determined in rat brain tissue during and after unilateral middle cerebral artery occlusion (MCAo). Cerebral lactate (Lac) as determined by 1H NMR spectroscopy, water diffusion, and T1, were quantified as well. Lac concentrations were used to estimate intracellular pH (pHi) in the brain during the MCA occlusion. A decrease in APTR during occlusion indicated acidification from 7.1 to 6.79 ± 0.19 (a drop by 0.3 ± 0.2 pH units), whereas pHi computed from Lac concentration was 6.3 ± 0.2 (a drop by 0.8 ± 0.2 pH units). Despite the disagreement between the two methods in terms of the size of the change in the absolute pHi during ischemia, ,APTR and pHi (and Lac concentration) displayed a strong correlation during the MCAo. Diffusion and T1, indicated cytotoxic edema following MCA occlusion; however, APTR returned slowly toward the values determined in the contralateral hemisphere post-ischemia. These data argue that the APTR during ischemia is affected not only by pHi but by other physicochemical factors as well, and indicates different aspects of pathology in the post-ischemic brain compared to those that influence water diffusion and T1,. Magn Reson Med 57:647,653, 2007. © 2007 Wiley-Liss, Inc. [source] | ||||||||||