| http://purl.uniprot.org/citations/15739255 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15739255 | http://www.w3.org/2000/01/rdf-schema#comment | "Elevated fibrinogen (Fg) concentration in blood is a high risk factor for many cardiovascular diseases. We hypothesize that Fg and its early degradation product, fragment D, may result in arterial constriction by binding endothelial intercellular adhesion molecule-1 (ICAM-1). The vasoconstriction induced by Fg and fragment D was studied in third- and second-order arterioles (3As and 2As, respectively) of Sprague-Dawley rat cremaster muscle in vivo, in aortic and femoral artery rings, and in the segments of first-order arterioles (1As) isolated from rat cremaster muscle. Intravascular infusion of Fg induced significant constriction of 3As and 2As (by 33.4 +/- 3.4 and 23.7 +/-4.3%, respectively) in vivo and was abolished in the presence of the specific endothelin type A receptor blocker BQ-610. Fg and fragment D produced significant constriction of both aortic and femoral artery rings. Isolated 1As constricted in response to Fg (0.3 microM) and fragment D (3 microM) by 31 +/-1.4 and 12 +/-1.5%, respectively. Fluorescently labeled Fg and fragment D bound to the vascular wall, whereas albumin bound to a significantly lesser degree. The binding of Fg and fragment D to the arteriolar wall and constriction of aortic and femoral artery rings as well as isolated 1As were abolished in the presence of anti-Fg and anti-ICAM-1 antibodies. These results indicate that binding of Fg and fragment D to the vascular wall through ICAM-1 may contribute to the increased vascular tone and resistance that compromise circulation."xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpheart.00856.2004"xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/author | "Sen U."xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/author | "D'Souza S.E."xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/author | "Falcone J.C."xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/author | "Lominadze D."xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/author | "Tsakadze N."xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/name | "Am J Physiol Heart Circ Physiol"xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/pages | "H1257-64"xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/title | "Fibrinogen and fragment D-induced vascular constriction."xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://purl.uniprot.org/core/volume | "288"xsd:string |
| http://purl.uniprot.org/citations/15739255 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15739255 |
| http://purl.uniprot.org/citations/15739255 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15739255 |
| http://purl.uniprot.org/uniprot/P02675#attribution-8FD13C0C5AF999E05A4DEF3889548485 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/15739255 |
| http://purl.uniprot.org/uniprot/P02671#attribution-8FD13C0C5AF999E05A4DEF3889548485 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/15739255 |
| http://purl.uniprot.org/uniprot/P02679#attribution-8FD13C0C5AF999E05A4DEF3889548485 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/15739255 |