Sandbox Reserved 1174: Difference between revisions

When an injury occurs LPA is released in the body.  LPA will then activate G-protein-coupled receptors.  Within the nervous system, LPA plays a role in the nociceptive process (nociceptive pain is a sharp pain that can come from a mild burn or twisted ankle).  The LPA signaling will activate GTPase RhoA <ref name= "Inoue">.  Once activated Rho translocates to the plasma membrane.  Rho will activate Rho kinase (ROCK) <ref name= "Inoue">.  The actiavtion of ROCK is a required step in the pathway in the stimulation of neurotic pain.  When ROCK was inhibited the remaining pathway no longer functioned normally.  Mice with the deletion of LPA₁ receptors had lower levels of pain <ref name= "Inoue"> DOI:10.1038/nm1060 </ref>.   

Idiopathic pulmonary fibrosis (IPF) has high rates of mortality <ref name= "Tager"> PMID:18066075 </ref>.  Understanding how LPA can effect fibrosis, is an important factor to finding medication and a cure for this disease.  The pathway of LPA-LPA₁ is important in mediating fibroblast migration and [https://en.wikipedia.org/wiki/Wound_healing Wound Healing].  Once fibrosis has been contracted LPA levels increase in the bronchoalveolar lavage (BAL) fluid.  The study showed that mice lacking LPA₁ had protection from mortality and were able to survive fibrosis.  LPA₁ plays an active role between lung injury and contracting pulmonary fibrosis.  The absence of LPA results in a vascular leak after an initial injury, leading to fibrosis.  LPA₁ is a link between lung injury and  [http://www.nature.com/nm/journal/v14/n1/fig_tab/nm1685_F4.html pulmonary fibrosis] <ref name= "Tager"/>.