PubMed:22007835 JSON TXT

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PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":396,"end":413},"obj":"HP_0002637"},{"id":"T2","span":{"begin":579,"end":596},"obj":"HP_0002637"},{"id":"T3","span":{"begin":637,"end":654},"obj":"HP_0002637"},{"id":"T4","span":{"begin":1486,"end":1503},"obj":"HP_0002637"},{"id":"T5","span":{"begin":1870,"end":1887},"obj":"HP_0002637"}],"text":"Caveolin-1 regulates nitric oxide-mediated matrix metalloproteinases activity and blood-brain barrier permeability in focal cerebral ischemia and reperfusion injury.\nThe roles of caveolin-1 (cav-1) in regulating blood-brain barrier (BBB) permeability are unclear yet. We previously reported that cav-1 was down-regulated and the production of nitric oxide (NO) induced the loss of cav-1 in focal cerebral ischemia and reperfusion injury. The present study aims to address whether the loss of cav-1 impacts on BBB permeability and matrix metalloproteinases (MMPs) activity during cerebral ischemia-reperfusion injury. We found that focal cerebral ischemia-reperfusion down-regulated the expression of cav-1 in isolated cortex microvessels, hippocampus, and cortex of ischemic brain. The down-regulation of cav-1 was correlated with the increased MMP-2 and -9 activities, decreased tight junction (TJ) protein zonula occludens (ZO)-1 expression and enhanced BBB permeability. Treatment of N(G) -nitro-L-arginine methyl ester [L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor] reserved the expression of cav-1, inhibited MMPs activity, and reduced BBB permeability. To elucidate the roles of cav-1 in regulating MMPs and BBB permeability, we used two approaches including cav-1 knockdown in cultured brain microvascular endothelial cells (BMECs) in vitro and cav-1 knockout (KO) mice in vivo. Cav-1 knockdown remarkably increased MMPs activity in BMECs. Meanwhile, with focal cerebral ischemia-reperfusion, cav-1 deficiency mice displayed higher MMPs activities and BBB permeability than wild-type mice. Interestingly, the effects of L-NAME on MMPs activity and BBB permeability was partly reversed in cav-1 deficiency mice. These results, when taken together, suggest that cav-1 plays important roles in regulating MMPs activity and BBB permeability in focal cerebral ischemia and reperfusion injury. The effects of L-NAME on MMPs activity and BBB permeability are partly mediated by preservation of cav-1."}

Allie

UseCases_ArguminSci_Discourse

{"project":"UseCases_ArguminSci_Discourse","denotations":[{"id":"T1","span":{"begin":0,"end":165},"obj":"DRI_Background"},{"id":"T2","span":{"begin":166,"end":267},"obj":"DRI_Background"},{"id":"T3","span":{"begin":268,"end":437},"obj":"DRI_Outcome"},{"id":"T4","span":{"begin":438,"end":616},"obj":"DRI_Challenge"},{"id":"T5","span":{"begin":617,"end":781},"obj":"DRI_Outcome"},{"id":"T6","span":{"begin":782,"end":907},"obj":"DRI_Approach"},{"id":"T7","span":{"begin":908,"end":924},"obj":"Token_Label.OUTSIDE"},{"id":"T8","span":{"begin":925,"end":973},"obj":"DRI_Approach"},{"id":"T9","span":{"begin":974,"end":1175},"obj":"DRI_Background"},{"id":"T10","span":{"begin":1176,"end":1402},"obj":"DRI_Outcome"},{"id":"T11","span":{"begin":1403,"end":1463},"obj":"DRI_Outcome"},{"id":"T12","span":{"begin":1464,"end":1613},"obj":"DRI_Background"},{"id":"T13","span":{"begin":1614,"end":1734},"obj":"DRI_Outcome"},{"id":"T14","span":{"begin":1735,"end":1911},"obj":"DRI_Challenge"},{"id":"T15","span":{"begin":1912,"end":2017},"obj":"DRI_Background"}],"text":"Caveolin-1 regulates nitric oxide-mediated matrix metalloproteinases activity and blood-brain barrier permeability in focal cerebral ischemia and reperfusion injury.\nThe roles of caveolin-1 (cav-1) in regulating blood-brain barrier (BBB) permeability are unclear yet. We previously reported that cav-1 was down-regulated and the production of nitric oxide (NO) induced the loss of cav-1 in focal cerebral ischemia and reperfusion injury. The present study aims to address whether the loss of cav-1 impacts on BBB permeability and matrix metalloproteinases (MMPs) activity during cerebral ischemia-reperfusion injury. We found that focal cerebral ischemia-reperfusion down-regulated the expression of cav-1 in isolated cortex microvessels, hippocampus, and cortex of ischemic brain. The down-regulation of cav-1 was correlated with the increased MMP-2 and -9 activities, decreased tight junction (TJ) protein zonula occludens (ZO)-1 expression and enhanced BBB permeability. Treatment of N(G) -nitro-L-arginine methyl ester [L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor] reserved the expression of cav-1, inhibited MMPs activity, and reduced BBB permeability. To elucidate the roles of cav-1 in regulating MMPs and BBB permeability, we used two approaches including cav-1 knockdown in cultured brain microvascular endothelial cells (BMECs) in vitro and cav-1 knockout (KO) mice in vivo. Cav-1 knockdown remarkably increased MMPs activity in BMECs. Meanwhile, with focal cerebral ischemia-reperfusion, cav-1 deficiency mice displayed higher MMPs activities and BBB permeability than wild-type mice. Interestingly, the effects of L-NAME on MMPs activity and BBB permeability was partly reversed in cav-1 deficiency mice. These results, when taken together, suggest that cav-1 plays important roles in regulating MMPs activity and BBB permeability in focal cerebral ischemia and reperfusion injury. The effects of L-NAME on MMPs activity and BBB permeability are partly mediated by preservation of cav-1."}

PubMed_ArguminSci

{"project":"PubMed_ArguminSci","denotations":[{"id":"T1","span":{"begin":166,"end":267},"obj":"DRI_Background"},{"id":"T2","span":{"begin":268,"end":437},"obj":"DRI_Outcome"},{"id":"T3","span":{"begin":438,"end":616},"obj":"DRI_Challenge"},{"id":"T4","span":{"begin":617,"end":781},"obj":"DRI_Outcome"},{"id":"T5","span":{"begin":782,"end":907},"obj":"DRI_Approach"},{"id":"T6","span":{"begin":925,"end":973},"obj":"DRI_Approach"},{"id":"T7","span":{"begin":974,"end":1175},"obj":"DRI_Background"},{"id":"T8","span":{"begin":1176,"end":1402},"obj":"DRI_Outcome"},{"id":"T9","span":{"begin":1403,"end":1463},"obj":"DRI_Outcome"},{"id":"T10","span":{"begin":1464,"end":1613},"obj":"DRI_Background"},{"id":"T11","span":{"begin":1614,"end":1734},"obj":"DRI_Outcome"},{"id":"T12","span":{"begin":1735,"end":1911},"obj":"DRI_Challenge"},{"id":"T13","span":{"begin":1912,"end":2017},"obj":"DRI_Background"}],"text":"Caveolin-1 regulates nitric oxide-mediated matrix metalloproteinases activity and blood-brain barrier permeability in focal cerebral ischemia and reperfusion injury.\nThe roles of caveolin-1 (cav-1) in regulating blood-brain barrier (BBB) permeability are unclear yet. We previously reported that cav-1 was down-regulated and the production of nitric oxide (NO) induced the loss of cav-1 in focal cerebral ischemia and reperfusion injury. The present study aims to address whether the loss of cav-1 impacts on BBB permeability and matrix metalloproteinases (MMPs) activity during cerebral ischemia-reperfusion injury. We found that focal cerebral ischemia-reperfusion down-regulated the expression of cav-1 in isolated cortex microvessels, hippocampus, and cortex of ischemic brain. The down-regulation of cav-1 was correlated with the increased MMP-2 and -9 activities, decreased tight junction (TJ) protein zonula occludens (ZO)-1 expression and enhanced BBB permeability. Treatment of N(G) -nitro-L-arginine methyl ester [L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor] reserved the expression of cav-1, inhibited MMPs activity, and reduced BBB permeability. To elucidate the roles of cav-1 in regulating MMPs and BBB permeability, we used two approaches including cav-1 knockdown in cultured brain microvascular endothelial cells (BMECs) in vitro and cav-1 knockout (KO) mice in vivo. Cav-1 knockdown remarkably increased MMPs activity in BMECs. Meanwhile, with focal cerebral ischemia-reperfusion, cav-1 deficiency mice displayed higher MMPs activities and BBB permeability than wild-type mice. Interestingly, the effects of L-NAME on MMPs activity and BBB permeability was partly reversed in cav-1 deficiency mice. These results, when taken together, suggest that cav-1 plays important roles in regulating MMPs activity and BBB permeability in focal cerebral ischemia and reperfusion injury. The effects of L-NAME on MMPs activity and BBB permeability are partly mediated by preservation of cav-1."}