| First Author | Yamagishi-Kimura R | Year | 2018 |
| Journal | Sci Rep | Volume | 8 |
| Issue | 1 | Pages | 11098 |
| PubMed ID | 30038227 | Mgi Jnum | J:269671 |
| Mgi Id | MGI:6271670 | Doi | 10.1038/s41598-018-29273-1 |
| Citation | Yamagishi-Kimura R, et al. (2018) Contribution of prostanoid FP receptor and prostaglandins in transient inflammatory ocular hypertension. Sci Rep 8(1):11098 |
| abstractText | We explored the involvement of FP receptor and endogenous prostaglandins (PGs) in transient ocular hypertension (OH) induced by PGE2 or PGF2alpha in mouse eyes. PGE2 and PGF2alpha 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 PGF2alpha 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 PGF2alpha on the increase in IOP were significantly weaker than those of PGE2, especially in EP1KO and EP3KO mice. Transient OH induced by PGE2 and PGF2alpha was significantly attenuated by nepafenac treatment in FPKO mice. Transient OH was induced by PGE2 and PGF2alpha 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 naive physiological role in the eye, and could regulate IOP elevation during PG-associated ocular inflammation. |
