Roles of sphingosine-1-phosphate signaling in angiogenesis

来源 :World Journal of Biological Chemistry | 被引量 : 0次 | 上传用户:chenyi686
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Sphingosine-1-phosphate (S1P) is a blood-borne lipid mediator with pleiotropic biological activities. S1P acts via the specific cell surface G-protein-coupled receptors, S1P1-5. S1P1 and S1P2 were originally identified from vascular endothelial cells (ECs) and smooth muscle cells, respectively. Emerging evidence shows that S1P plays crucial roles in the regulation of vascular functions, including vascular formation, barrier protection and vascular tone via S1P1, S1P2 and S1P3. In particular, S1P regulates vascular formation through multiple mechanisms; S1P exerts both positive and negative effects on angiogenesis and vascular maturation. The positive and negative effects of S1P are mediated by S1P1 and S1P2, respectively. These effects of S1P1 and S1P2 are probably mediated by the S1P receptors expressed in multiple cell types including ECs and bone-marrow-derived cells. The receptor-subtype-specific, distinct effects ofS1P favor the development of novel therapeutic tactics for antitumor angiogenesis in cancer and therapeutic angiogenesis in ischemic diseases. Sphingosine-1-phosphate (S1P) is a blood-borne lipid mediator with pleiotropic biological activities. S1P acts via the specific cell surface G-protein-coupled receptors, S1P1-5. S1P1 and S1P2 were originally identified from vascular endothelial cells Emerging evidence shows that S1P plays a crucial role in the regulation of vascular functions, including vascular formation, barrier protection and vascular tone via S1P1, S1P2 and S1P3. The positive and negative effects of S1P are mediated by S1P1 and S1P2, respectively. These effects of S1P1 and S1P2 are probably mediated by the S1P receptors expressed in multiple cell types including ECs and bone-marrow-derived cells. The receptor-subtype-specific, distinct effects of S1P favor the development of novel therapeutic tactics for antitum or angiogenesis in cancer and therapeutic angiogenesis in ischemic diseases.
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