Contribution of prostanoid FP receptor and prostaglandins in transient inflammatory ocular hypertension.
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ABSTRACT: We explored the involvement of FP receptor and endogenous prostaglandins (PGs) in transient ocular hypertension (OH) induced by PGE2 or PGF2? in mouse eyes. PGE2 and PGF2? were topically applied to induce transient OH in Wild-type (WT) and FP-, EP1-, EP2-, and EP3-deficient (knockout [KO]) mice. To suppress endogenous PG production, the non-steroidal anti-inflammatory drug nepafenac was applied topically before treatment. PGE2 and PGF2? induced significant OH in the WT, FPKO, and EP1-3KO mice compared to the control 30?min after instillation, and the increase in IOP at 30 or 60?min after instillation in FPKO mice was significantly higher than that in the WT mice. The effects of PGF2? on the increase in IOP were significantly weaker than those of PGE2, especially in EP1KO and EP3KO mice. Transient OH induced by PGE2 and PGF2? was significantly attenuated by nepafenac treatment in FPKO mice. Transient OH was induced by PGE2 and PGF2? in WT, FPKO, and EP1-3KO mice, which was enhanced in FPKO mice. This OH was significantly diminished by nepafenac treatment in FPKO mice, suggesting that FP receptor may have an important naïve physiological role in the eye, and could regulate IOP elevation during PG-associated ocular inflammation.
SUBMITTER: Yamagishi-Kimura R
PROVIDER: S-EPMC6056481 | biostudies-other | 2018 Jul
REPOSITORIES: biostudies-other
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