| http://purl.uniprot.org/citations/15678112 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15678112 | http://www.w3.org/2000/01/rdf-schema#comment | "We previously demonstrated that pharmacological inhibition of Na(+)-K(+)-Cl-cotransporter isoform 1 (NKCC1) is neuroprotective in in vivo and in vitro ischemic models. In this study, we investigated whether genetic ablation of NKCC1 provides neuroprotection after ischemia. Focal ischemia was induced by 2 hours occlusion of the left middle cerebral artery (MCAO) followed by 10 or 24 hours reperfusion. Two hours MCAO and ten or twenty-four hours reperfusion caused infarction (approximately 85 mm3) in NKCC1 wild-type (NKCC1(+/+)) mice. Infarction volume in NKCC1(-/-) mice was reduced by approximately 30% to 46%. Heterozygous mutant (NKCC1(+/-)) mice showed approximately 28% reduction in infarction (P>0.05). Two hours MCAO and twenty-four hours reperfusion led to a significant increase in brain edema in NKCC1(+/+) mice. In contrast, NKCC1(+/-) and NKCC1(-/-) mice exhibited approximately 50% less edema (P<0.05). Moreover, white matter damage was assessed by immunostaining of amyloid precursor protein (APP). An increase in APP was detected in NKCC1(+/+) mice after 2 hours MCAO and 10 hours reperfusion. However, NKCC1(-/-) mice exhibited significantly less APP accumulation (P<0.05). Oxygen-glucose deprivation (OGD) induced approximately 67% cell death and a fourfold increase in Na+ accumulation in cultured NKCC1(+/+) cortical neurons. OGD-mediated cell death and Na+ influx were significantly reduced in NKCC1(-/-) neurons (P<0.05). In addition, inhibition of NKCC1 by bumetanide resulted in similar protection in NKCC1(+/+) neurons and astrocytes (P<0.05). These results imply that stimulation of NKCC1 activity is important in ischemic neuronal damage."xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.org/dc/terms/identifier | "doi:10.1038/sj.jcbfm.9600006"xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/author | "Chen H."xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/author | "Luo J."xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/author | "Sun D."xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/author | "Shull G.E."xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/author | "Kintner D.B."xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/name | "J Cereb Blood Flow Metab"xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/pages | "54-66"xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/title | "Na(+)-dependent chloride transporter (NKCC1)-null mice exhibit less gray and white matter damage after focal cerebral ischemia."xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://purl.uniprot.org/core/volume | "25"xsd:string |
| http://purl.uniprot.org/citations/15678112 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15678112 |
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| http://purl.uniprot.org/uniprot/Q3TP36 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/15678112 |
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