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Abstract
Lysophospholipid (LP) research has experienced a period of renaissance with the discovery of the lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) receptors in the late 1990s. Vertebrate LP receptors regulate embryogenesis, vascular development, neurogenesis, uterine development, oocyte survival, immune cell trafficking and inflammatory reactions. LP signaling is important in cancer, autoimmunity and inflammatory diseases. Research on LP biology has contributed to the development of a first-generation S1P receptor modulator that has entered phase III clinical trials for the treatment of multiple sclerosis. Further basic research on LP signaling is anticipated to lead to novel therapeutic tools to combat various human diseases.
Highlights
Lysophospholipid (LP) research has experienced a period of renaissance with the discovery of the lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) receptors in the late 1990s
A major advance in the LP field occurred with the demonstration that the effects of LPA required the action of heterotrimeric G proteins [3]
Independent studies from our laboratory demonstrated that the G protein-coupled receptor EDG-1 is a Gi-coupled high affinity S1P receptor [5]
Summary
S1P receptors regulate important physiological functions of the vascular system, such as vascular morphogenesis and maturation, cardiac function, vascular permeability, and tumor angiogenesis [13]. S1P3 receptor confers cardioprotection in a mouse model for ischemia-reperfusion, caused by coronary artery occlusion followed by reperfusion In this model, S1P2,3 receptor double null mice display significantly increased infarct size and compromised survival of endothelial cells and cardiomyocytes [29]. S1P2,3 receptor double null mice display significantly increased infarct size and compromised survival of endothelial cells and cardiomyocytes [29] These studies suggest that cooperative and/or antagonistic signaling between S1P receptor subtypes influence pathological angiogenesis, permeability, wound healing, and other clinical syndromes associated with cancer, sepsis, stroke, and heart disease. Autotoxin deficient mice die at early embryonic development due to impaired blood vessel formation in both yolk sac and embryo, suggesting functional redundancy among the LPA receptors expressed in the mouse vascular system [32]. Such defects are noted in patients suffering from illnesses such as schizophrenia and Alzheimers disease
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