作者: Stacey A. Langan , Gerard B. Nash , Steve P. Watson , Leyre Navarro-Núñez
DOI: 10.1160/TH13-01-0060
关键词:
摘要: CLEC-2 is a C-type lectin receptor which highly expressed on platelets but also found at low levels different immune cells. elicits powerful platelet activation upon engagement by its endogenous ligand, the mucin-type glycoprotein podoplanin. Podoplanin in variety of tissues, including lymphatic endothelial cells, kidney podocytes, type I lung epithelial lymph node stromal cells and choroid plexus epithelium. Animal models have shown that correct separation blood vasculatures during embryonic development dependent CLEC-2-mediated activation. Additionally, podoplanin-deficient mice show abnormalities heart, lungs, lymphoid whereas absence affects brain development. This review summarises current understanding molecular pathways regulating podoplanin function suggests other physiological pathological processes where this interaction might exert crucial roles.