The present research is focused on providing new insights in the pathophysiological functions of enteric glia identifying novel molecular target for the intervention of gastrointestinal disorders. Specifically, we focused on the role of two different glial mediators: S100B and PGE2. S100B is a calciumbinding protein physiologically release by EGCs acting as neurotrophic factor.
An aberrant production of S100B represents a key step in several intestinal diseases, including ulcerative colitis, celiac diseases and melanoma. However, evidences about the implication of S100B in colon cancer outcome are still missing. On the other hand, PGE2 is a bioactive lipid belonging to prostanoid family exhibiting different actions in intestinal inflammation, tissue repair as well as colon cancer. Although the involvement of PGE2 in the homeostasis and pathological conditions of gastrointestinal tract is well established, any investigations about PGE2 as glial mediator have been reported yet. In this scenario, the present study aimed to:
i) elucidate the role of S100B in ex vivo culture of human colorectal cancer;
ii) evaluate the impact of glial-derived PGE2 on intestinal functions in both
physiological and pathological conditions in mPGES1-S100B-deleted mice
