EXPLORING THE POSSIBLE ROLE OF C3aR LIGATION ON INTESTINAL EPITHELIAL CELLS
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There is growing evidence that complement is activated during inflammatory gastrointestinal disease but there is a deficit in our understanding of roles the anaphylatoxin C3a may have on intestinal epithelial cells (IECs). We have identified mRNA and protein for the C3a receptor (C3aR) in the IEC lines T84 and HT-29, as well as in freshly isolated murine colonic epithelium. We have identified Gαi as the G protein through which C3aR signals, and activation of the downstream signaling molecules Ras, C-Raf, ERK1/2 and activation of Nuclear Factor κB. We found that C3a increased mRNA levels of the chemokine CXCL2. We propose a role for C3a in which this split complement protein is pro-survival in the gut and helps promote wound healing while priming IECs for subsequent inflammation based on findings that indicate C3a influences IEC secretion of angiogenin and insulin-like growth factor binding protein 1.