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Contents 1 Comparison of S1P and LPA 2 Function 3 Relevance 4 Clinical Testing 4.1 Pain

Comparison of S1P and LPA

Lysophosphatidic Acid Receptors (LPA) are part of a larger family known as lysophospholipid receptor family (EDG family). Within this family there is a structure called S1P1. Since only the structures for LPA₁ and S1P₁ are known in the EDG family, comparisons are made between the two structures ^[2].

There is a difference in binding paths between these two receptors. The binding path in the LPA₁ is located in the extracellular milieu. While in the S1P₁ the ligands are able to have access to the membrane so that the binding can occur. There is a difference in the shape of the electron density from the binding pocket. In S1P₁ the binding pocket has more of an oval shape. For the LPA₁ receptor the binding pocket has a spherical shape. Since the binding pocket is more spherical it gives LPA₁ the ability to be able to recognize a larger group of chemical species. In particular the ability to bind with acyl chains of varying lengths ^[2].

Function

Relevance

Clinical Testing

LPA is still in the clinical stage of testing. So far the LPA receptors have had physiological effects on every organism that it has been tested with. There have been studies done looking at what happens with infertility, fibrosis, pain, and cancer when they come into contact with LPA receptors ,ref name= "Chrencik"/>. LPA receptors are commonly found in serum and saliva. ^[1].

Pain

LPA, a signaling phospholipid, that attaches to three specific G-protein-coupled receptors. After an injury occurs LPA is released in the body. It then will activate G-protein-coupled receptors. Mice without the LPA₁ receptors were studied to see the role that LPA signaling played in controlling pain. LPA can activate multiple pathways in particular, Ras and Pho which belong to the family of GTPases ^[3]. Another use of LPA is it can help in stimulation of cell migration ^[1]. It was seen that with targeted deletion of LPA receptors the mice would be cured from fibrosis. Mice who had fibrosis were given LPA1 regulated LPA-induced fibroblast. Over time the mice who had fibrosis began to have their lungs repaired. The amount of fluid in their lungs decreased.