October 1992
Volume 33, Issue 11
Free
Articles  |   October 1992
cAMP production via the adenylyl cyclase pathway is reduced in RCS rat RPE.
Author Affiliations
  • C Y Gregory
    Jules Stein Eye Institute, UCLA School of Medicine 90024-7008.
  • T A Abrams
    Jules Stein Eye Institute, UCLA School of Medicine 90024-7008.
  • M O Hall
    Jules Stein Eye Institute, UCLA School of Medicine 90024-7008.
Investigative Ophthalmology & Visual Science October 1992, Vol.33, 3121-3124. doi:
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      C Y Gregory, T A Abrams, M O Hall; cAMP production via the adenylyl cyclase pathway is reduced in RCS rat RPE.. Invest. Ophthalmol. Vis. Sci. 1992;33(11):3121-3124.

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Abstract

cAMP production was investigated in retinal pigment epithelium (RPE) cells isolated from normal rats and from rats with an inherited retinal dystrophy (Rdy/p+). In normal RPE cells, 5'-[N-Ethylcarboxamido]-adenosine (A2 receptors) produced a fivefold increase in the level of cyclic adenosine monophosphate (cAMP) over basal levels. However, only a onefold increase in cAMP was observed in dystrophic cells. cAMP production by prostaglandins E1 and E2 (prostaglandin receptors) in dystrophic RPE cells was only 29-38% of the level observed in normal cells. Direct stimulation of adenylyl cyclase by 10 mumol/l forskolin increased cAMP levels in normal RPE cells by 90 fold over basal, but only by sixfold in the dystrophic cells. These data suggest there may be a defect in the adenylyl cyclase signaling pathway in dystrophic RPE cells.

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