MCG 101 tumors implanted on prostaglandin receptor EP2 wildtype and EP2 knockout mice
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PROVIDER: PRJNA794813 | ENA |
REPOSITORIES: ENA
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Project description:IL-23 induces ptgs2 encoding cyclooxygenase 2 in Th17 cells and produces PGE2, which acts back on PGE2 receptors EP2 and EP4 in these cells and enhances IL-23-induced expression of an IL-23 receptor subunit gene, Il23r, by activating STAT3, CREB1 and NF-κB through cAMP-protein kinase A signaling. This PGE2 signaling also induces expression of various inflammation-related genes, which possibly function in Th17 cell-mediated pathology. Combined deletion of EP2 and EP4 selectively in T cells suppressed accumulation of IL-17A+ and IL-17A+IFN-γ+ pathogenic Th17 cells and abolished skin inflammation in IL-23-induced psoriasis mouse model. Analysis of human psoriatic skin biopsies shows positive correlation between PGE2 signaling and the IL-23/Th17 pathway.
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Project description:To understand the role of prostaglandin (PG) receptor EP2 (Ptger2) signaling in ovulation and fertilization, we investigated time-dependent expression profiles in wild-type (WT) and Ptger2-/- cumuli before and after ovulation by using microarrays. We used Affymetrix U74A ver2 microarrays to investigate gonadotropin-induced gene expression profiles in WT and EP2KO cumulus cells before and after ovulation. Immature mice were primed with pregnant mare serum gonadotropin (PMSG) as an FSH-like stimulation. The cumulus-oocyte complexes (COCs) were isolated from mice 48 h after PMSG injection (H0) and from PMSG-primed mice exposed to human chorionic gonadotropin (hCG) as an LH-like stimulation for 3, 9 or 14 h (H3, H9 or H14, respectively).
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