Background
We previously studied the metabolomics, transcriptomics and proteomics of intestinal tissue of Hirschsprung disease (HSCR) patients; the
Conclusions
MPGES-1 derived PGE2 inhibits the cell migration by regulating ARP2/3 complex via prostaglandin E2 receptor. Potential mechanisms are the damage of cytoskeleton and related proteins leading to failure of cell polarize and migration. Here we thoroughly inquire the role mPGES-1 derived PGE2 plays in cell migration which might provide a new thinking in the investigation interrelated to the pathogenesis of HSCR.
Methods
SH-SY5Y and SK-N-BE2 cell lines were obtained from American Type Culture Collection (ATCC, USA). Prostaglandin E2 and its synthetase inhibitors were purchased from Med Chem Express (MCE, USA). Migration assays were performed with transwell and scratch assays. Cell proliferation was confirmed by CCK8 method. Flow cytometer was used to detect the cell cycle and cell apoptosis. The expressions of mRNA and protein of EP2, ARP2/3 were determined by qRT-PCR and western blot respectively. Immunofluorescence and confocal laser scanning microscopy were used to observe the morphology and function of cytoskeleton.
Results
MPGES-1 derived PGE2 decreased the relative expression of EP2 and ARP2/3 and caused damage to cytoskeleton. As to cell functions, PGE2 inhibited cell migration while having no effects on the proliferation, cell cycle and apoptosis. By adding mPGES-1 inhibitor MK886 the abnormal expression and damaged cell function were reversed. Conclusions: MPGES-1 derived PGE2 inhibits the cell migration by regulating ARP2/3 complex via prostaglandin E2 receptor. Potential mechanisms are the damage of cytoskeleton and related proteins leading to failure of cell polarize and migration. Here we thoroughly inquire the role mPGES-1 derived PGE2 plays in cell migration which might provide a new thinking in the investigation interrelated to the pathogenesis of HSCR.