作者: Mizuho Hasegawa , Charles A. Parkos , Asma Nusrat
DOI: 10.1016/J.AJPATH.2020.06.005
关键词:
摘要: N-formyl peptide receptors (FPRs) serve as phagocyte pattern-recognition that play a crucial role in the regulation of host defense against infection. Epithelial cells also express FPRs, and their activation during inflammation or injury results enhanced epithelial migration proliferation improved mucosal wound repair. However, signaling mechanisms govern FPR1 activity are not well understood. This study identified novel FPR1-interacting protein, WD40 repeat protein (WDR)-26, which negatively regulates FPR1-mediated healing intestinal cells. We show WDR26-mediated inhibition repair is mediated through Rac family small GTPase 1 cell division cycle 42 activation, downstream intracellular reactive oxygen species production. Furthermore, on with N-formyl-methionyl-leucyl phenylalanine, WDR26 dissociates from FPR1, resulting 42/Rac signaling, increased migration, These findings elucidate regulatory function