Journal
PLATELETS
Volume 27, Issue 8, Pages 743-750Publisher
TAYLOR & FRANCIS INC
DOI: 10.3109/09537104.2016.1171834
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Funding
- NHLBI NIH HHS [R01 HL112248] Funding Source: Medline
- NIDDK NIH HHS [R01 DK054254, R01 DK124126, R01 DK083850] Funding Source: Medline
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Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is an Ig-ITIM superfamily member that regulates integrin alpha(II)beta 3 function. We hypothesized that its twin protein, CEACAM2, exerts a similar physiologic role in murine platelets. CEACAM2-deficient mice (Cc2(-/-)) displayed prolonged tail bleeding times and increased volume of blood loss. Cc2(-/-) platelets have moderate integrin alpha(II)beta 3-mediated functional defects with impaired kinetics of platelet spreading on fibrinogen and type I collagen and delayed kinetics in the retraction of fibrin clots in vitro. This functional integrin alpha(II)beta 3 defect could not be attributed to altered integrin alpha(II)beta 3 expression. Cc2(-/-) platelets displayed normal 'inside-out' signaling properties as demonstrated by normal agonist-induced binding of soluble fluorescein isothiocyanate (FITC)-fibrinogen and JON/A antibody binding. This data provides direct evidence that disruption of CEACAM2 induces a moderate integrin alpha(II)beta 3-mediated platelet function defect, and that CEACAM2 is essential to maintain a normal integrin alpha(II)beta 3-mediated platelet function.
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