Tang Zhaoming, Kattula Sravya, Holle Lori A, Cooley Brian C, Lin Feng-Chang, Wolberg Alisa S
Department of Pathology and Laboratory Medicine University of North Carolina at Chapel Hill Chapel Hill NC USA.
Department of Biostatistics and North Carolina Translational and Clinical Sciences Institute University of North Carolina at Chapel Hill Chapel Hill NC USA.
Res Pract Thromb Haemost. 2019 Nov 6;4(1):111-116. doi: 10.1002/rth2.12278. eCollection 2020 Jan.
The compositions of venous (red blood cell-rich) and arterial (platelet-rich) thrombi are mediated by distinct pathophysiologic processes; however, fibrin is a major structural component of both. The transglutaminase factor XIII (FXIII) stabilizes fibrin against mechanical and biochemical disruption and promotes red blood cell retention in contracted venous thrombi. Previous studies have shown factor XIII (FXIII) inhibition decreases whole blood clot mass and therefore, may be a therapeutic target for reducing venous thrombosis. The role of FXIII in arterial thrombogenesis is less studied, and the particular contribution of platelet FXIII remains unresolved.
To determine whether FXIII reduction prevents experimental arterial thrombogenesis.
Using wild-type mice and mice with genetically imposed deficiency in FXIII, we measured thrombus formation and stability following ferric chloride-induced arterial thrombosis. We also determined the impact of FXIII on the mass of contracted platelet-rich plasma clots.
Following vessel injury, , , and mice developed occlusive arterial thrombi. FXIII deficiency did not significantly reduce the incidence or prolong the time to occlusion. FXIII deficiency also did not alter the timing of reflow events or decrease platelet-rich clot mass.
FXIII does not significantly alter the underlying pathophysiology of experimental arterial thrombus formation.
静脉血栓（富含红细胞）和动脉血栓（富含血小板）的组成由不同的病理生理过程介导；然而，纤维蛋白是两者的主要结构成分。转谷氨酰胺酶因子 XIII（FXIII）可稳定纤维蛋白，防止其受到机械和生化破坏，并促进红细胞滞留在收缩的静脉血栓中。先前的研究表明，抑制因子 XIII（FXIII）可降低全血凝块质量，因此，可能是减少静脉血栓形成的治疗靶点。FXIII 在动脉血栓形成中的作用研究较少，血小板 FXIII 的具体贡献仍未明确。
确定 FXIII 减少是否能预防实验性动脉血栓形成。
使用野生型小鼠和基因敲除 FXIII 的小鼠，我们测量了氯化铁诱导的动脉血栓形成后的血栓形成和稳定性。我们还确定了 FXIII 对收缩的富含血小板血浆凝块质量的影响。
血管损伤后，野生型小鼠、杂合子小鼠和纯合子小鼠均形成闭塞性动脉血栓。FXIII 缺乏并未显著降低血栓形成的发生率或延长闭塞时间。FXIII 缺乏也未改变再流事件的时间或降低富含血小板凝块的质量。
FXIII 不会显著改变实验性动脉血栓形成的潜在病理生理学。
