Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we tested the hypothesis that the Angiopoietin 1 (Ang1)/Tie2 pathway mediates simvastatin-induced vascular integrity and migration of neuroblasts after stroke. Rats were subjected to 2 hrs of middle cerebral artery occlusion (MCAo) and treated, starting 1 day after stroke with or without simvastatin (1 mg/kg, daily) for 7 days. Simvastatin treatment significantly decreased blood-brain barrier (BBB) leakage and concomitantly, increased Ang1, Tie2 and Occludin expression in the ischaemic border (IBZ) compared to the MCAo control group. Simvastatin also significantly increased doublecortin (DCX, a marker of migrating neuroblasts) expression in the IBZ compared to control MCAo rats. DCX was highly expressed around vessels. To further investigate the signalling pathway of simvastatin-induced vascular stabilization and angiogenesis, rat brain microvascular endothelial cell (RBMEC) culture was employed. The data show that simvastatin treatment of RBMEC increased Ang1 and Tie2 gene and protein expression and promoted phosphorylated-Tie2 activity. Simvastatin significantly increased endothelial capillary tube formation, an index of angiogenesis, compared to non-treated control. Inhibition of Ang1 or knockdown of Tie2 gene expression in endothelial cells significantly attenuated simvastatin-induced capillary tube formation. In addition, simvastatin significantly increased subventricular zone (SVZ) explant cell migration compared to non-treatment control. Inhibition of Ang1 significantly attenuated simvastatin-induced SVZ cell migration. Simvastatin treatment of stroke increases Ang1/Tie2 expression and thereby reduces BBB leakage and promotes vascular stabilization. Ang1/Tie2 expression induced by simvastatin treatment promotes neuroblast micro-vascular coupling after stroke.
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PMID:Increasing Ang1/Tie2 expression by simvastatin treatment induces vascular stabilization and neuroblast migration after stroke. 1854 44

In experimental models, growth factors (GFs) such as vascular endothelial growth factor (VEGF), Angiopoietin 1 (Ang-1), or granulocyte-colony stimulating factor (G-CSF) mediate brain recovery after intracerebral hemorrhage (ICH). Our aim was to study the association between serum levels of GF and clinical outcome in patients with ICH. A total of 95 patients with primary ICH (male, 66.3%; mean age, 67.8+/-9.8 years) were prospectively included in the study within 12 h from symptoms onset. The main outcome variable was good functional outcome at 3 months (modified Rankin scale < or =2). Median serum levels of GF at 72 h from stroke onset were significantly higher in patients with good outcome (n=39) compared with those with poor outcome (all P<0.0001). Serum levels of VEGF > or =330 pg/mL, G-CSF > or =413 pg/mL, and Ang-1 > or =35 ng/mL at 72 h were independently associated with good functional outcome (odds ratio (OR), 11.2; 95% confidence interval (CI): 2.9 to 43.0; OR, 19.6; 95% CI: 3.9 to 97.9; and OR, 14.7; 95% CI: 3.6 to 60.0, respectively), neurologic improvement (all P<0.0001) and reduced residual cavity at 3 months (all P<0.01). These results illustrate that high serum levels of GF are associated with good functional outcome and reduced lesion volume in ICH.
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PMID:High serum levels of growth factors are associated with good outcome in intracerebral hemorrhage. 1975 22