Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo.

Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo. Research Abstract Details 

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Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo. Abstract Text:

Sarmina Hassan,Irma M Sainz,Mohammad M Khan,Harlan N Bradford,Irma Isordia-Salas,Sakeen W Kashem,R Balfour Sartor,Robert W Colman,

High-molecular-weight kininogen (HK) and its domain 3 (D3) exhibit anticoagulant properties and inhibit platelet activation at low thrombin concentration in vitro. We hypothesized that the rapid occlusive thrombosis in HK-deficient (HKd) rats following endothelial injury of the aorta results from enhanced platelet aggregation by thrombin. The effects of D3 (G235-M357) or D3-derived peptides on thrombosis in vivo were tested. D3 and its exon 7C terminal peptide (E7CP, K270-Q292), expressed as glutathione S-transferase (GST) fusion proteins (GST-D3, GST-E7CP), or GST alone, as well as cleaved HK (HKa) or synthetic peptide E7CP, were infused intravenously 10 min before endothelial injury. Blood flow was reduced down to 10% of baseline flow within 28 +/- 5.2 min by a platelet-fibrin thrombus in GST-treated HKd rats compared with >240 min in GST-treated normal HK rats (wild type). GST-D3, GST-E7CP, HKa, or E7CP infusion prolonged the flow time to 233, >240, 223, and >240 min, respectively, in HKd rats. When GST-E7CP was infused 10 min after the injury, blood flow was maintained for >240 min. Thrombin-antithrombin concentrations were elevated by injury in HKd rats receiving GST from 35 to 55 microg/l and decreased with GST-E7CP, HKa, or E7CP reconstitution to 40, 15, and 9 microg/l, respectively. We conclude that HKd rats are prothrombotic and that HKa, kininogen D3, and its fragment E7CP modulate arterial thrombosis after endothelial injury.

Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo. Publishing Authors By Initials

S Hassan,IM Sainz,MM Khan,HN Bradford,I Isordia-Salas,SW Kashem,RB Sartor,RW Colman,

For similar cardiovascular diseases: vascular diseases: embolism and thrombosis: thrombosis research abstracts see: cardiovascular diseases: vascular diseases: embolism and thrombosis: thrombosis research

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Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Heart and circulat

VOLUME: 292

Page Numbers: H2959-65

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 9

MONTH: 02

YEAR: 2007

Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901228

Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo. Keywords Mesh Terms:

KEYWORDS: Thrombosis

MESH TERMS: prevention & control

Chemical & Substance for Abstract: Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo. Information

Substance Name: Thrombin

Registry Number: EC 3.4.21.5

Grant and Affiliation Information for Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo.

AFFILIATION: Sol Sherry Thrombosis Research Center, Temple Univeristy School of Medicine, 3400 N. Broad St., Rm. 418 OMS, Philadelphia, PA 19140, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: T32 HL0077713

ACRONYM: HL

MEDLINETA: Am J Physiol Heart Circ Physio

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