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Titolo:
Impaired platelet prostacyclin receptor activity: a monozygotic twin studydiscordant for spinal cord injury
Autore:
Kahn, NN; Sinha, AK; Bauman, WA;
Indirizzi:
Vet Affairs Med Ctr, Spinal Corp Injury Serv, Spinal Corp Damage Res Ctr, Bronx, NY 10468 USA Vet Affairs Med Ctr Bronx NY USA 10468 amage Res Ctr, Bronx, NY 10468 USA CUNY Mt Sinai Sch Med, New York, NY 10029 USA CUNY Mt Sinai Sch Med New York NY USA 10029 h Med, New York, NY 10029 USA
Titolo Testata:
CLINICAL PHYSIOLOGY
fascicolo: 1, volume: 21, anno: 2001,
pagine: 60 - 66
SICI:
0144-5979(200101)21:1<60:IPPRAA>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIC-HEART-DISEASE; HUMAN-BLOOD-PLATELETS; ADENYLATE-CYCLASE; RISK-FACTORS; INSULIN; BINDING; ACTIVATION; MEMBRANE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Kahn, NN Vet Affairs Med Ctr, Spinal Corp Injury Serv, Spinal Corp Damage Res Ctr, Room IE-02,130 W Kingsbridge Rd, Bronx, NY 10468 USA Vet Affairs Med Ctr Room IE-02,130 W Kingsbridge Rd Bronx NY USA 10468
Citazione:
N.N. Kahn et al., "Impaired platelet prostacyclin receptor activity: a monozygotic twin studydiscordant for spinal cord injury", CLIN PHYSL, 21(1), 2001, pp. 60-66

Abstract

Coronary artery disease (CAD) has been reported to occur prematurely in individuals with spinal cord injury (SCI). Although persons with SCI have metabolic abnormalities that may predispose them to CAD, other potential aetiologies may also be operative. Increased platelet aggregation, among other factors, initiates thrombus formation at the site of the vessel injury, which may acutely obstruct arterial blood flow. Prostacyclin is known to have abeneficial effect to inhibit platelet aggregation and prevent thrombus formation. Platelets were studied from 12 pairs of monozygotic twins, one co-twin with SCI. Each twin pair had similar patterns of platelet aggregation with adenosine diphosphate (ADP), thrombin or collagen, as well as inhibition of platelet aggregation by prostacyclin (PGE(1)/I-2) and synthesis of cyclic adenosine mono phosphate (AMP) by the prostanoid. However, the twin pairs differed in their response to PGE(1)/I-2 inhibition of platelet-stimulated thrombin generation that was completely inhibited in non-SCI platelets but not in SCI platelets. Scatchard analysis of the binding of H-3-prostaglandin E-1, a stable prostacyclin receptor probe, showed the presence of one high-affinity (K-d1 = 8.1 +/- 2.8 nM; n(l) = 168 +/- 35 sites per platelet)and one low-affinity (K-d2 = 1.1 +/- 0.22 muM; n(2) = 1772 +/- 220 sites per cell) prostacyclin receptor in normal platelets, whereas in SCI platelets there was a significant loss (P <0.00l) of high-affinity receptor sites (K-d1 = 6.34 +/- 1.80 nM; n(1) = 42 +/- 11 sites per platelet) with no significant change in the low-affinity receptor sites (K-d2 = 1.2 +/- 0.23 muM; n(2) = 1860 +/- 412 sites per cell). These discordant platelet findings in identical twin pairs raises the possibility of an environmental aetiology for accelerated CAD in those with SCI. The loss of inhibitory effect of PGI(2) on thrombin generation in the twin with SCI appears to be because of loss of platelet high-affinity prostanoid receptors, which may contribute to atherogenesis in individuals with SCI.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 18:18:09