March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Effect of Oleoylethanolamide on Aqueous Humor Outflow
Author Affiliations & Notes
  • Akhilesh Kumar
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Zhuanhong Qiao
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Pritesh P. Kumar
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Zhao-Hui Song
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Footnotes
    Commercial Relationships  Akhilesh Kumar, None; Zhuanhong Qiao, None; Pritesh P. Kumar, None; Zhao-Hui Song, None
  • Footnotes
    Support  NIH Grants EY13632 and DA11551
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 1989. doi:
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      Akhilesh Kumar, Zhuanhong Qiao, Pritesh P. Kumar, Zhao-Hui Song; Effect of Oleoylethanolamide on Aqueous Humor Outflow. Invest. Ophthalmol. Vis. Sci. 2012;53(14):1989.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To study the effects of oleoylethanolamide (OEA) on aqueous humor outflow via the trabecular meshwork pathway.

Methods: : The effects of OEA on aqueous humor outflow via the trabecular meshwork pathway were measured using a porcine anterior segment perfused organ culture model. Different concentrations of OEA were administered to the perfusion medium and the aqueous humor outflow facility was monitored for 5 hours. SR141716A, SR144528, O-1918, and GW6471 were administered to anterior segment to determine the involvement of various receptors on the outflow effects of OEA. PD98059, an inhibitor of the p42/44 MAP kinase pathway , was used to examine the involvement of the MAP kinase signal transduction pathway in regulating OEA induced enhancement of outflow facility. OEA induced activation of p42/44 MAP kinase was determined by western blot analysis using an anti-phospho p42/44 MAP kinase antibody.

Results: : Administration of OEA caused a concentration-dependent enhancement of aqueous humor outflow facility, with the maximum effect (162.4 ± 15.3 % of basal outflow facility) achieved at 2 hour after the administration of 30 nM of OEA. Pretreatment with either 1 µM SR144528 or 3 µM GW6471 produced a partial antagonism on the OEA-induced increased aqueous humor outflow facility. However, pretreatment with either 1 µM O-1918 or 1 µM SR141716A had no effect on OEA induced enhancement of aqueous humor outflow facility. Treatment of trabecular meshwork cells with OEA for 10 min activated phosphorylation of p42/44 MAP kinase, which was blocked by pretreatment with either GW6471 or SR144528. Furthermore, PD98059, an inhibitor of the p42/44 MAP kinase pathway, blocked both OEA-induced phosphorylation of p42/44 MAP kinase and enhancement of aqueous humor outflow facility.

Conclusions: : The results from this study demonstrate that OEA increases aqueous humor outflow through the trabecular meshwork pathway and these effects may be mediated by PPARα and non-CB1/CB2 cannabinoid receptors through activation of p42/44 MAP kinase.

Keywords: outflow: trabecular meshwork • signal transduction • receptors 
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