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Title: Platelet fibrinogen binding in Basset Hound Hereditary Thrombopathy

Abstract

Platelets from dogs with Basset Hound Hereditary Thrombopathy (BHT) display a thrombasthenia-like aggregation defect but have been shown to have normal amounts of platelet membrane glycoproteins IIb and IIIa (GP IIb-IIIa). In order to investigate the possibility of a functionally abnormal GPIIb-IIIa complex, which might be unable to bind fibrinogen after stimulation, fibrinogen binding in BHT was evaluated. Two canine fibrinogen preparations were used, one from BHT dogs and one from normal control dogs, as well as a human fibrinogen preparation. Platelets from BHT and normal dogs were activated with 1 x 10/sup -5/M ADP in the presence of /sup 125/I-labeled fibrinogen and the surface bound radioactivity quantitated. For all fibrinogen preparations, the amount of fibrinogen bound by BHT platelets was not significantly different than that bound by normal dog platelets. BHT platelets bound 23,972 +/- 3612 and normal dog platelets bound 23,033 +/- 3971 molecules of fibrinogen per platelet. The BHT platelet aggregation defect does not seem to be caused by a functionally abnormal GP IIb-IIIa complex, since BHT platelets bind normal amounts of fibrinogen. The results suggest that fibrinogen binding is not sufficient for platelet aggregation, and other factors, perhaps receptor mobility and membrane phospholipid content should bemore » investigated in BHT.« less

Authors:
; ; ;
Publication Date:
Research Org.:
Michigan State Univ., East Lansing
OSTI Identifier:
5390116
Report Number(s):
CONF-8604222-
Journal ID: CODEN: FEPRA; TRN: 86-028508
Resource Type:
Conference
Journal Name:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
Additional Journal Information:
Journal Volume: 45:3; Conference: 70. annual meeting of the Federation of American Society for Experimental Biology, St. Louis, MO, USA, 13 Apr 1986
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; FIBRINOGEN; BIOCHEMICAL REACTION KINETICS; ADP; BLOOD PLATELETS; DOGS; GLUCOPROTEINS; HEREDITARY DISEASES; IODINE 125; RECEPTORS; TRACER TECHNIQUES; ANIMALS; BETA DECAY RADIOISOTOPES; BIOLOGICAL MATERIALS; BLOOD; BLOOD CELLS; BLOOD COAGULATION FACTORS; BODY FLUIDS; CARBOHYDRATES; COAGULANTS; DAYS LIVING RADIOISOTOPES; DISEASES; DRUGS; ELECTRON CAPTURE RADIOISOTOPES; GLOBULINS; HEMATOLOGIC AGENTS; HEMOSTATICS; INTERMEDIATE MASS NUCLEI; IODINE ISOTOPES; ISOTOPE APPLICATIONS; ISOTOPES; KINETICS; MAMMALS; MATERIALS; MEMBRANE PROTEINS; NUCLEI; NUCLEOTIDES; ODD-EVEN NUCLEI; ORGANIC COMPOUNDS; PROTEINS; RADIOISOTOPES; REACTION KINETICS; SACCHARIDES; VERTEBRATES; 550901* - Pathology- Tracer Techniques

Citation Formats

Patterson, W, Estry, D, Schwartz, K, and Bell, T. Platelet fibrinogen binding in Basset Hound Hereditary Thrombopathy. United States: N. p., 1986. Web.
Patterson, W, Estry, D, Schwartz, K, & Bell, T. Platelet fibrinogen binding in Basset Hound Hereditary Thrombopathy. United States.
Patterson, W, Estry, D, Schwartz, K, and Bell, T. 1986. "Platelet fibrinogen binding in Basset Hound Hereditary Thrombopathy". United States.
@article{osti_5390116,
title = {Platelet fibrinogen binding in Basset Hound Hereditary Thrombopathy},
author = {Patterson, W and Estry, D and Schwartz, K and Bell, T},
abstractNote = {Platelets from dogs with Basset Hound Hereditary Thrombopathy (BHT) display a thrombasthenia-like aggregation defect but have been shown to have normal amounts of platelet membrane glycoproteins IIb and IIIa (GP IIb-IIIa). In order to investigate the possibility of a functionally abnormal GPIIb-IIIa complex, which might be unable to bind fibrinogen after stimulation, fibrinogen binding in BHT was evaluated. Two canine fibrinogen preparations were used, one from BHT dogs and one from normal control dogs, as well as a human fibrinogen preparation. Platelets from BHT and normal dogs were activated with 1 x 10/sup -5/M ADP in the presence of /sup 125/I-labeled fibrinogen and the surface bound radioactivity quantitated. For all fibrinogen preparations, the amount of fibrinogen bound by BHT platelets was not significantly different than that bound by normal dog platelets. BHT platelets bound 23,972 +/- 3612 and normal dog platelets bound 23,033 +/- 3971 molecules of fibrinogen per platelet. The BHT platelet aggregation defect does not seem to be caused by a functionally abnormal GP IIb-IIIa complex, since BHT platelets bind normal amounts of fibrinogen. The results suggest that fibrinogen binding is not sufficient for platelet aggregation, and other factors, perhaps receptor mobility and membrane phospholipid content should be investigated in BHT.},
doi = {},
url = {https://www.osti.gov/biblio/5390116}, journal = {Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)},
number = ,
volume = 45:3,
place = {United States},
year = {Sat Mar 01 00:00:00 EST 1986},
month = {Sat Mar 01 00:00:00 EST 1986}
}

Conference:
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