Investigating the role of how S1PR3 promotes the release of CGRP
Psoriasis is an autoimmune disease that causes skin cells to grow at an abnormal rate. This disease leads the skin to develop red bumpy patches covered with white scales. Itchiness, burns, and stings are common discomforts associated with the disease. Psoriasis affects 8 million Americans and 125 million people worldwide.
Currently, antihistamine does not treat psoriasis. Our lab has been exploring non-histamine dependent pathways of itch. Recent work in the Bautista Lab (Hill et al., 2018) identified Sphingosine 1-Phosphate Receptor 3 (S1PR3) as a key signaling molecule that promotes itch-evoked scratching behaviors in mice. However, it is still unknown if S1PR3 activation promotes the release of inflammatory mediators that trigger itch and inflammation. Calcitonin Gene Related Peptide (CGRP) is one inflammatory mediator elevated in Psoriatic skin that recruits and activates immune cells. My research will seek to identify the role of how S1PR3 promotes the release of CGRP from itch neurons and drives inflammation in the skin. This research will provide new insight into the mechanisms that may trigger the inflammatory response of psoriatic skin.
Message to Sponsor
- Major: Cell & Developmental Biology
- Sponsor: Rose Hills Independent
- Mentor: Diana Bautista