Venous thrombi, fibrin- and rbc-rich clots triggered by inflammation and blood stasis, underlie devastating, and sometimes fatal, occlusive events. During intravascular fibrin deposition, rbc are thought to become passively trapped in thrombi and therefore have not been considered a modifiable thrombus component. In the present study, we determined that activity of the transglutaminase factor XIII (FXIII) is critical for rbc retention within clots and directly affects thrombus size. Compared with WT mice, mice carrying a homozygous mutation in the fibrinogen γ chain (
Maria M. Aleman, James R. Byrnes, Jian-Guo Wang, Reginald Tran, Wilbur A. Lam, Jorge Di Paola, Nigel Mackman, Jay L. Degen, Matthew J. Flick, Alisa S. Wolberg
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