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 Blood, 1 May 2004, Vol. 103, No. 9, pp. 3396-3402.
Prepublished online as a Blood First Edition Paper on January 22, 2004; DOI 10.1182/blood-2003-10-3721.

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Submitted November 4, 2003
Accepted December 29, 2003

Genetic Variation Responsible for Mouse Strain Differences in Integrin {alpha}2 Expression Is Associated with Altered Platelet Responses to Collagen

Tong-Tong Li, Susana Larrucea, Shiloe Souza, Suzanne M Leal, Jose A Lopez, Edward M Rubin, Bernhard Nieswandt, and Paul F Bray*

Medicine, Baylor College of Medicine, Houston, TX, USA
Genetics, Baylor College of Medicine, Houston, TX, USA
Lawrence Berkeley Laboratories, Berkeley, CA, USA
Vascular Biology, Rudolf Virchow Center, Wurzburg, Germany

* Corresponding author; email: pbray{at}bcm.tmc.edu.

As mouse models have become commonplace for studying hemostasis and thrombosis, we considered whether the mouse system had utility for assessing genetic alterations in platelet receptors. Platelets from 5 mouse strains (C57BL/6 [C57], FVB/N [FVB], BALB/c, C3H/He and 129Sv) showed only minor differences in the expression of integrin {alpha}IIb, integrin {beta}3, GPIb{alpha} or GPVI across strains. However, FVB platelets expressed ~50% the level of integrin {alpha}2 as platelets from other strains (P<0.0001). We bred FVB mice with C57 and assessed {alpha}2 expression in FVB/C57xFVB/C57 (F2) offspring. Linkage analysis demonstrated the gene responsible for {alpha}2 levels is tightly linked to the D13mit260 marker (lod score 6.7) near the {alpha}2 gene. FVB platelets showed reduced aggregation and a longer lag phase to collagen. FVB and C57 platelets aggregated similarly to collagen related peptide, but FVB platelets showed a reduction in rhodocytin-induced Syk and PLC{gamma}2 tyrosine phosphorylation. Thus, FVB platelets express half the level of {alpha}2 as other mouse strains, a trait linked to the {alpha}2 gene and seemingly responsible for reduced platelet aggregation to collagen. These strain differences serve as a useful model for the two-fold difference in human platelet {alpha}2{beta}1 expression and demonstrate that {alpha}2{beta}1 participates in signaling during platelet activation.


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