Does plexin-B1, a semaphorin 4D receptor, play a role in thrombosis?

摘要

Mechanisms of platelet activation and aggregation are fairly well defined. However, questions still remain regarding interactions that occur after platelet activation. Among others, Brass et al. investigated aspects of this area (for reviews see [1,2]). One particular protein of interest is semaphorin 4D which acts as a ligand for CD72 and plexin-Bl receptors on platelets. Cleavage and shedding of semaphorin 4D allows stimulation of platelets and other nearby cells [3]. These platelet-platelet interactions favor thrombus formation and growth. Zhu et al. demonstrated impaired platelet responses in semaphorin 4D-deficient mice. Aggregation was reduced -75% in semaphorin 4D-deficient platelets in response to suboptimal collagen concentration, and the aggregation response to convulxin (GPV1 collagen receptor ligand) was also decreased. A modest anti-thrombotic effect of semaphorin 4D deletion in mice was reported in FeQ3-induced arterial injury with a more marked effect in laser-induced arteriolar injury [3]. Yukawa et al. (2010) reported that plaque growth was reduced in semaphorin 4D deficient mice [4].