Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Platelet-stimulated thrombin and PDGF are normalized by insulin and Ca2+ channel blockers
Autore:
Kahn, NN;
Indirizzi:
Vet Adm Med Ctr, Spinal Cord Damage Res Ctr, Bronx, NY 10468 USA Vet Adm Med Ctr Bronx NY USA 10468 rd Damage Res Ctr, Bronx, NY 10468 USA CUNY Mt Sinai Sch Med, Dept Med, New York, NY 10029 USA CUNY Mt Sinai Sch Med New York NY USA 10029 t Med, New York, NY 10029 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
fascicolo: 5, volume: 39, anno: 1999,
pagine: E856 - E862
SICI:
0193-1849(199905)39:5<E856:PTAPAN>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROSTAGLANDIN-E1/I2 RECEPTOR ACTIVITY; ISCHEMIC-HEART-DISEASE; GROWTH-FACTOR; PROSTACYCLIN RECEPTORS; ADENYLATE-CYCLASE; INHIBITION; NUCLEOTIDES; AGGREGATION; ACTIVATION; MEMBRANE;
Keywords:
receptor; prostacyclin; prostaglandin E-1; coronary artery disease; platelet-derived growth factor adenosine 3 ',5 ',-cyclic monophosphate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Kahn, NN Vet2,dm Med Ctr, Spinal Cord Damage Res Ctr, 130 W Kingsbridge Rd,Room 1E-0 Vet Adm Med Ctr 130 W Kingsbridge Rd,Room 1E-02 Bronx NY USA 10468
Citazione:
N.N. Kahn, "Platelet-stimulated thrombin and PDGF are normalized by insulin and Ca2+ channel blockers", AM J P-ENDO, 39(5), 1999, pp. E856-E862

Abstract

Coronary artery disease is accelerated in chronic spinal cord injury (SCI). Because prostacyclin (PGI(2)) may retard atherogenesis through its inhibitory effects on platelet function, the role of PGI(2) on SCI platelets was determined. The SCI platelets were neither hypersensitive to aggregating agonists nor resistant to the inhibitory effect of PGI(2), but PGI(2) failed to inhibit platelet-stimulated thrombin generation and the release of platelet-derived growth factor (PDGF) in SCI. Because thrombin and PDGF are atherogenic mitogens, the generation of these mitogens was investigated. Both the release of PDGF and thrombin generation in SCT platelets were higher when compared with control (n = 12). Treatment of non-SCI platelets with 100 nM PGE(1) (a stable probe of PGI(2)) inhibited the release of the mitogens by 90% (P < 0.001), with no effect on SCI platelets. Scatchard analysis of prostaglandin E-1 (PGE(1)) binding showed a 70% decrease of PGI(2) receptorson the SCI platelet surface. Treatment of SCI platelets with insulin or Ca2+ channel blockers restored the PGI(2)-receptor number and "normalized" the inhibition of PDGF release and thrombin generation by PGI(2).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 11:58:19