Topic
Beta-thromboglobulin
About: Beta-thromboglobulin is a research topic. Over the lifetime, 540 publications have been published within this topic receiving 19856 citations. The topic is also known as: beta-thromboglobulin.
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TL;DR: It is concluded that cardiopulmonary bypass patients demonstrate abnormal clinical bleeding when there is a persistence of platelet dysfunction manifested as a bleeding time of greater than 20 mm after protamine administration and such bleeding patients with a prolonged bleeding time should receive platelet transfusions.
716 citations
TL;DR: Measurement of plasma levels of two secreted platelet proteins has been suggested as a means for detecting increased platelet activation in vivo and it appears that when there is increased release of beta- thromboglobulin and platelet factor 4 in vivo, there is an increase in the ratio of plasma beta-thrombglobulin to plasma plateletFactor 4 compared to that found in normal individuals.
482 citations
TL;DR: This study investigated the hypothesis that patients suffering from ischemic heart disease and depression concurrently may have abnormal platelet activation resulting in an increased risk of thrombosis.
348 citations
TL;DR: Plasma β-TG appears to equilibrate with synovial and amniotic fluids, but the PF4 concentration in these fluids is lower than in plasma, and neither protein passes freely into the cerebrospinal fluid.
275 citations
TL;DR: In vivo several alpha granule proteins released from platelets may affect wound healing by causing directed fibroblast migration through chemotactic activity of platelet factor 4, PDGF, and beta-thromboglobulin.
Abstract: At sites of blood vessel injury, platelets release numerous substances that may have biological activities influencing cellular responses. In this study we examined separately the chemotactic activity for fibroblasts of three highly purified proteins obtained from platelet alpha granules: platelet factor 4 (PF4), platelet-derived growth factor (PDGF), and beta-thromboglobulin (BTG). We observed that each of these proteins was strongly chemotactic for fibroblasts, with maximum chemotactic activity in each instance comparable to that observed with an optimal concentration of the control chemotactic protein, plasma fibronectin. Each protein was active at very low concentrations. The peak chemotactic activities of PF4, PDGF, and BTG occurred at 200 mg/ml, 30 ng/ml, and 6 ng/ml, respectively. Specificity of fibroblast chemotaxis to individual platelet proteins was provided by finding that anti-PF4 immunoglobulin blocked the chemotactic activity of PF4 without affecting the chemotactic activity of PDGF, while anti-PDGF immunoglobulin blocked the activity of PDGF but did not alter the capacity of PF4 to promote fibroblast chemotaxis. These results suggest that in vivo several alpha granule proteins released from platelets may affect wound healing by causing directed fibroblast migration.
268 citations