| http://purl.uniprot.org/citations/21168935 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21168935 | http://www.w3.org/2000/01/rdf-schema#comment | "Breakdown of the inner blood-retinal barrier and the blood-brain barrier is associated with changes in tight and adherens junction-associated proteins that link vascular endothelial cells. This study aimed to test the hypothesis that transforming growth factor (TGF)-β1 increases the paracellular permeability of vascular endothelial monolayers through tyrosine phosphorylation of VE-cadherin and claudin-5. Bovine retinal and human brain capillary endothelial cells were grown as monolayers on coated polycarbonate membranes. Paracellular permeability was studied by measuring the equilibration of (14)C-inulin or fluorescence-labelled dextran. Changes in VE-cadherin and claudin-5 expression were studied by immunocytochemistry (ICC) and quantified by cell-based enzyme linked immunosorbent assays (ELISA). Tyrosine phosphorylation of VE-cadherin and claudin-5 was studied by ICC, immunoprecipitation and Western blotting. We found that exposure of endothelial cells to TGF-β1 caused a dose-dependent increase in paracellular permeability as reflected by increases in the equilibration of (14)C-inulin. This effect was enhanced by the tyrosine phosphatase inhibitor orthovanadate and attenuated by the tyrosine kinase inhibitor lavendustin A. ICC and cell-based ELISA revealed that TGF-β1 induced both dose- and time-dependent decreases in VE-cadherin and claudin-5 expression. Assessment of cell viability indicated that changes in these junction-associated proteins were not due to endothelial death or injury. ICC revealed that tyrosine phosphorylation of endothelial monolayers was greatly enhanced by TGF-β1 treatment, and immunoprecipitation of cell lysates showed increased tyrosine phosphorylation of VE-cadherin and claudin-5. Our results suggest that tyrosine phosphorylation of VE-cadherin and claudin-5 is involved in the increased paracellular permeability of central nervous system-derived vascular endothelium induced by TGF-β1."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ejcb.2010.10.013"xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Li S."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Shen W."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Zhu L."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Chung S.H."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Su T."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Gillies M.C."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Couraud P.O."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Romero I.A."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Weksler B."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/author | "Stayt J."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/name | "Eur J Cell Biol"xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/pages | "323-332"xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/title | "Tyrosine phosphorylation of VE-cadherin and claudin-5 is associated with TGF-beta1-induced permeability of centrally derived vascular endothelium."xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://purl.uniprot.org/core/volume | "90"xsd:string |
| http://purl.uniprot.org/citations/21168935 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21168935 |
| http://purl.uniprot.org/citations/21168935 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21168935 |
| http://purl.uniprot.org/uniprot/P33151#attribution-F959B3E539BC37EB708FF52A4885804D | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21168935 |
| http://purl.uniprot.org/uniprot/O00501#attribution-F959B3E539BC37EB708FF52A4885804D | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21168935 |
| http://purl.uniprot.org/uniprot/P01137#attribution-F959B3E539BC37EB708FF52A4885804D | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/21168935 |
| http://purl.uniprot.org/uniprot/#_D3DX19-mappedCitation-21168935 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21168935 |
| http://purl.uniprot.org/uniprot/#_O00501-mappedCitation-21168935 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21168935 |