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Omidenepag, a non-prostanoid EP2 receptor agonist, induces enlargement of the 3D organoid of 3T3-L1 cells

ABSTRACT: 2D and 3D cultures of 3T3-L1 cells were employed in a study of the effects of Omidenepag (OMD), interacting with a non-prostanoid EP2 receptor, on adipogenesis. Upon adipogenesis, the effects on lipid staining, the mRNA expression of adipogenesis-related genes (Ppar?, CEBPa, Ap2, and Glut4) and the extracellular matrix (ECM) including collagen type 1, 4 and 6, and fibronectin, and the size and physical property of 3D organoids were compared between groups that had been treated with EP2 agonists (butaprost and OMD) and PGF2?. Upon adipogenesis, these significantly suppressed lipid staining and the mRNA expression of related genes. EP2 agonists and PGF2? influenced the mRNA expression of ECM in different manners, and these effects were also different between 2 and 3D cultures. Examining the physical properties by a microsqueezer indicated that the solidity of the 3D organoids became significantly lowered upon adipogenesis and these effects were not affected by EP2 agonists. In contrast, 3D organoid stiffness was markedly enhanced by the presence of PGF2?. These observations indicate that EP2 agonists affect the adipogenesis of 3T3-L1 cells in different manners, as compared to PGF2?, suggesting that OMD may not induce PGF2? related orbital fat atrophy, called the deepening of the upper eyelid sulcus (DUES).

SUBMITTER: Ida Y

PROVIDER: S-EPMC7524797 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Project description:ObjectivesWe evaluated early medication persistence with new topical antiglaucoma eyedrops, omidenepag isopropyl 0.002% (a selective prostaglandin EP2 agonist).Design and settingRetrospective two-institute study in Himeji and Akashi in Japan.ParticipantsWe analysed patients with glaucoma who were prescribed topical omidenepag isopropyl from November 2018 to December 2019. From the last outpatient visit of patients until February 2020, 235 patients were prescribed a new solution of omidenepag isopropyl (129 patients in the initial monotherapy group, 85 in the switching group (switched from another topical antiglaucoma eyedrops), 19 added to another topical antiglaucoma eyedrops group, and 2 were lost to follow-up)). Additionally, we recruited 98 patients (3 were lost to follow-up) who received initial latanoprost 0.005% monotherapy during the same period as a control group.OutcomesMedication persistence failure was defined as drug discontinuation due to any adverse effects or change of therapy. Kaplan-Meier survival analysis was performed with a Cox regression analysis.ResultsAmong 233 patients, 48 (20%) showed failure of treatment; the median persistence time of all patients was 165 days, and the median time until discontinuation of omidenepag isopropyl was 45 days. The total persistence rates were 85%, 80% and 70% at 3, 6 and 12 months, respectively. Risk factors for failure were male gender (HR: 1.45, p=0.023) and monotherapy/switching (HR: 1.715, p=0.002). Comparison between latanoprost and omidenepag isopropyl monotherapy, only male gender (HR: 1.43, p=0.016) was a significant risk factor. Failures associated with omidenepag isopropyl were due to insufficient intraocular pressure-lowering efficiency (n=26, observed during all the period), followed by conjunctival hyperaemia (n=10) and visual acuity disturbance (n=5) in patients who were observed until 3 months.ConclusionMedication persistence with omidenepag isopropyl is mostly positive; however, clinicians should also be cautious of early failure.

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Omidenepag, a non-prostanoid EP2 receptor agonist, induces enlargement of the 3D organoid of 3T3-L1 cells

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