Effect of Alpha2-Antiplasmin on Tissue Remodeling pp. 229-235
Authors: (Yosuke Kanno and Hiroyuki Matsuno—Dept. of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women’s Collage of Liberal Arts, Kyoto, Japan)
Abstract: The fibrinolytic system (Plasminogen/plasmin system) is supposed to play an important role in both the synthesis and degradation of extracellular matrices. However, the detailed mechanism on how this system affects tissue remodeling remains unclear. Inhibition of the system occurs either at the levels of plasminogen activator, regulated by specific plasminogen activator inhibitors (PAIs) or at the levels of plasmin, mainly regulated by alpha2-antiplasmin (2AP). 2AP is a specific plasmin inhibitor. We investigated the role of 2AP on tissue remodeling by using a wound-healing model and fibrosis model in both wild type mice and 2AP deficient (2AP-/-) mice. Our findings newly indicate that the absence of 2AP enhances the secretion of VEGF, and over secretion of VEGF promotes angiogenesis and wound healing. Moreover, the absence of 2AP attenuates bleomycin-induced fibrosis, and 2AP induces the production of TGF- These data suggest that 2AP plays an important role in wound healing and fibrosis. These findings indicate a potential new aspect in this field and could be a useful report on tissue remodeling.