Gregory C Y, Abrams T A, Hall M O
Jules Stein Eye Institute, UCLA School of Medicine 90024-7008.
Invest Ophthalmol Vis Sci. 1992 Oct;33(11):3121-4.
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.
对从正常大鼠以及患有遗传性视网膜营养不良（Rdy/p+）的大鼠中分离出的视网膜色素上皮（RPE）细胞中的环磷酸腺苷（cAMP）生成情况进行了研究。在正常RPE细胞中，5'-[N-乙基甲酰胺基]-腺苷（A2受体）使环磷酸腺苷（cAMP）水平相较于基础水平增加了五倍。然而，在营养不良的细胞中仅观察到cAMP水平增加了一倍。在营养不良的RPE细胞中，前列腺素E1和E2（前列腺素受体）所产生的cAMP仅为正常细胞中所观察到水平的29%-38%。用10微摩尔/升的福斯高林直接刺激腺苷酸环化酶，使正常RPE细胞中的cAMP水平相较于基础水平增加了90倍，但在营养不良的细胞中仅增加了六倍。这些数据表明，营养不良的RPE细胞中的腺苷酸环化酶信号通路可能存在缺陷。
