| http://purl.uniprot.org/citations/23006728 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23006728 | http://www.w3.org/2000/01/rdf-schema#comment | "Recent evidence suggested that ClC-3 channel/antiporter is involved in regulation of nuclear factor (NF)-κB activation. However, the mechanism explaining how ClC-3 modulates NF-κB signaling is not well understood. We hypothesized that ClC-3-dependent alteration of intracellular chloride concentration ([Cl(-)](i)) underlies the effect of ClC-3 on NF-κB activity in endothelial cells. Here, we found that reduction of [Cl(-)](i) increased tumor necrosis factor-α (TNFα)-induced expression of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 and adhesion of monocytes to endothelial cells (P<0.05; n=6). In Cl(-) reduced solutions, TNFα-evoked IκB kinase complex β and inhibitors of κBα phosphorylation, inhibitors of κBα degradation, and NF-κB nuclear translocation were enhanced. In addition, TNFα and interleukin 1β could activate an outward rectifying Cl(-) current in human umbilical vein endothelial cells and mouse aortic endothelial cells. Knockdown or genetic deletion of ClC-3 inhibited or abolished this Cl(-) conductance. Moreover, Cl(-) channel blockers, ClC-3 knockdown or knockout remarkably reduced TNFα-induced intercellular adhesion molecule 1 and vascular cell adhesion molecule 1expression, monocytes to endothelial cell adhesion, and NF-κB activation (P<0.01; n=6). Furthermore, TNFα-induced vascular inflammation and neutrophil infiltration into the lung and liver were obviously attenuated in ClC-3 knockout mice (P<0.01; n=7). Our results demonstrated that decrease of [Cl(-)](i) induced by ClC-3-dependent Cl(-) efflux promotes NF-κB activation and thus potentiates TNFα-induced vascular inflammation, suggesting that inhibition of ClC-3-dependent Cl(-) current or modification of intracellular Cl(-) content may be a novel therapeutic approach for inflammatory diseases."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.org/dc/terms/identifier | "doi:10.1161/hypertensionaha.112.198648"xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Liu J."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Tao J."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Yang H."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Shang F."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Huang L.Y."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Liang S.J."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Zeng D.Y."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Zhou J.G."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Wu Q.Q."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Tang Y.B."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Lv X.F."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Guan Y.Y."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Su Y.X."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Huang E.W."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/author | "Xiong L.X."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/name | "Hypertension"xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/pages | "1287-1293"xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/title | "Decrease of intracellular chloride concentration promotes endothelial cell inflammation by activating nuclear factor-kappaB pathway."xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://purl.uniprot.org/core/volume | "60"xsd:string |
| http://purl.uniprot.org/citations/23006728 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23006728 |
| http://purl.uniprot.org/citations/23006728 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23006728 |