Abstract
We explored the involvement of FP receptor and endogenous prostaglandins (PGs) in transient ocular hypertension (OH) induced by PGE2 or PGF2α in mouse eyes. PGE2 and PGF2α 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 PGF2α 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 PGF2α on the increase in IOP were significantly weaker than those of PGE2, especially in EP1KO and EP3KO mice. Transient OH induced by PGE2 and PGF2α was significantly attenuated by nepafenac treatment in FPKO mice. Transient OH was induced by PGE2 and PGF2α 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.
Highlights
It has long been reported that inflammation-inducing substances, referred to as ‘irins’, are present in the eye, most of which have been clarified to be the prostaglandins (PGs) PGE2 and PGF2α1
The intraocular pressure (IOP) increase by 0.01% PGE2 or PGF2α was minor compare to 0.1% of both drugs (Supplement Figure S1) we determined the dose for PGE2 and PGF2α as 0.1%
The IOPs at 30 min after instillation of the vehicle or 0.1% PGE2 were 12.8 ± 0.7 and 15.7 ± 0.7 mmHg, respectively, indicating that PGE2 significantly increased IOP compared to the control 30 min after instillation (p < 0.001) in WT mice (Fig. 1)
Summary
It has long been reported that inflammation-inducing substances, referred to as ‘irins’, are present in the eye, most of which have been clarified to be the prostaglandins (PGs) PGE2 and PGF2α1. Drugs and analogs related to PGs are currently the most commonly used agents to treat glaucoma and lower intraocular pressure (IOP), their physiological roles in the eye have not been fully clarified. We speculated that the FP receptor is unlikely to be involved in the maintenance of IOP under normal conditions, but rather may have an endogenous role in controlling IOP fluctuations in the case of ocular inflammation. We investigated the involvement of the FP receptor and endogenous PGs in transient ocular hypertension (OH) induced by PGE2 or PGF2α in mouse eyes
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
