April 1989
Volume 30, Issue 4
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Articles  |   April 1989
Arachidonic acid metabolism by cultured bovine corneal endothelial cells.
Author Affiliations
  • M E Gerritsen
    Department of Physiology, New York Medical College, Valhalla 10595.
  • J Rimarachin
    Department of Physiology, New York Medical College, Valhalla 10595.
  • C A Perry
    Department of Physiology, New York Medical College, Valhalla 10595.
  • B I Weinstein
    Department of Physiology, New York Medical College, Valhalla 10595.
Investigative Ophthalmology & Visual Science April 1989, Vol.30, 698-705. doi:
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      M E Gerritsen, J Rimarachin, C A Perry, B I Weinstein; Arachidonic acid metabolism by cultured bovine corneal endothelial cells.. Invest. Ophthalmol. Vis. Sci. 1989;30(4):698-705.

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

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Abstract

Pathways of arachidonic acid metabolism were identified in freshly prepared and in cultured bovine corneal endothelial cells. The principal pathway of arachidonic acid metabolism in the bovine corneal endothelial cells appears to be the cyclooxygenase pathway with the resultant synthesis of PGI2, PGF2 alpha and PGE2. At least two of these products, PGI2 and PGF2 alpha, are formed by the enzymatic conversion of the substrate, PGH2. Measurements of endogenous prostaglandin production by radioimmunoassay demonstrated that PGE2 was the major arachidonic acid metabolite released, with smaller amounts of PGF2 alpha and the stable hydrolysis product of PGI2, 6-keto PGF1 alpha. The release of all three prostanoids was significantly increased by the addition of the calcium ionophore (A23187), human thrombin, bradykinin and histamine. Basal and stimulated release of prostaglandins by the corneal endothelium may contribute to the regulation of intraocular pressure and also in the modulation of the corneal response to injury.

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