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Titolo:
Modulators of intraplatelet calcium concentration affect the binding of thrombospondin to blood platelets in healthy donors and patients with type 2 diabetes mellitus
Autore:
Wieclawska, B; Rozalski, M; Trojanowski, Z; Watala, C;
Indirizzi:
Med Univ Lodz, Lab Haemostasis & Haemostat Disorders, PL-90141 Lodz, Poland Med Univ Lodz Lodz Poland PL-90141 stat Disorders, PL-90141 Lodz, Poland
Titolo Testata:
EUROPEAN JOURNAL OF HAEMATOLOGY
fascicolo: 6, volume: 66, anno: 2001,
pagine: 396 - 403
SICI:
0902-4441(200106)66:6<396:MOICCA>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
MEMBRANE LIPID FLUIDITY; ACTIVATED PLATELETS; WHOLE-BLOOD; CD36; LEUKOCYTES; FIBRIN; CLOTS; IDDM;
Keywords:
thrombospondin (TSP); glycoprotein IV (CD36); platelet activation; calcium mobilisation; type 2 diabetes mellitus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Watala, C Med Univ Lodz, Lab Haemostasis & Haemostat Disorders, Ul Narutowicza 96, PL-90141 Lodz, Poland Med Univ Lodz Ul Narutowicza 96 Lodz PolandPL-90141 dz, Poland
Citazione:
B. Wieclawska et al., "Modulators of intraplatelet calcium concentration affect the binding of thrombospondin to blood platelets in healthy donors and patients with type 2 diabetes mellitus", EUR J HAEMA, 66(6), 2001, pp. 396-403

Abstract

Thrombospondin (TSP), which is secreted from or.-granules of activated platelets, binds to its surface receptor (CD36) in the presence of Ca2+. Objectives: We monitored how the modulation of intraplatelet Ca affects TSP binding to CD36 on platelets from healthy donors and patients xvith tyke 2 diabetes mellitus. We also aimed to verify whether the impaired Ca2+ mobilisation in diabetes influences TSP binding upon the pharmacological modulation of calcium transport. Methods: Whole blood cytometry was used to monitor TSPrelease/binding and CD36 presentation in platelets from 28 type 2 patientsand 33 healthy donors. Results: No significant changes in TSP and CD36 levels were revealed between the groups in circulating platelets and TRAP-, collagen- or thrombin-activated platelets. In healthy donors, 1 muM thapsigargin (TG) elevated the TRAP-activated TSP binding (by up to 50%, p <0.001), 5 mM EGTA reversed the effect (by up to 85%,p < 0.001), and overcame the effect of TG when used together. Less profoundly expressed effects occurred in the NIDDM group. In both groups TG increased the presentation of CD36 in TRAP-stimulated platelets (p < 0.05), whereas EGTA lowered the TRAP-stimulated increase in CD36 (p <0.001). The inhibition of CD36 by EGTA was stronger in healthy volunteers (41% vs. 32%, respectively, p < 0.05), whereas the activation by TG was higher in the NIDDM group (11% vs. 27%, p < 0.05). When acting together the suppressive effects of EGTA on TG-dependent Ca mobilisation were much attenuated in diabetic subjects (p < 0.05). Conclusion: Both the release of TSP and CD36 presentation are under the influence of agents modulating intracellular Ca2+. Diabetic platelets seem more vulnerable to the releasers of cytosolic [Ca2+] and more resistant to the blockers of cytosolic [Ca2+] mobilisation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/09/20 alle ore 22:01:27