Role of coagulation factor XIII in invasion of macrophages

利用FXIII （FXIII-A）缺陷小鼠的催化A亚基，研究了凝血因子XIII （FXIII）在巨噬细胞侵袭中的可能作用。fxiii - a缺陷巨噬细胞的趋化能力低于野生型细胞，尽管不是稳定的显著性。在脂多糖（LPS）处理的野生型小鼠的心脏组织中，型胶原短暂地增加了巨噬细胞侵袭的病变。相比之下，在LPS处理的fxiii - a缺陷小鼠心脏中，I型胶原的沉积几乎没有增加。因此，我们认为细胞内的FXIII-A参与了巨噬细胞的趋化作用，FXIII-A参与了损伤组织中I型胶原沉积的增加。

A possible role of coagulation factor XIII (FXIII) in invasion of macrophages was examinedusing catalytic A subunit of FXIII (FXIII-A)-deficient mice. FXIII-A-deficient macrophagesshowed lower chemotactic ability than wildtype cells, although it was not stationerysignificant. In the heart tissue of lipopolysaccharide (LPS)-treated wildtype mice, type Icollagen transiently increased lesions where macrophages invaded. In contrast, depositionof type I collagen hardly increased in heart of FXIII-A-deficient mice treated with LPS.Thus, it was suggested that FXIII-A inside cells involved in chemotaxis of macrophages,and FXIII-A contributed to increase of type I collagen deposition in damaged tissues.