A decreased Ca2+-wave propagation is found among cultured RPE cells from dystrophic RCS rats.
Invest Ophthalmol Vis Sci
; 39(8): 1493-502, 1998 Jul.
Article
em En
| MEDLINE
| ID: mdl-9660499
ABSTRACT
PURPOSE:
The authors investigated intercellular communication among cultured rat retinal pigment epithelial (RPE) cells isolated from dystrophic Royal College of Surgeons (RCS) rats by studying the conduction of the [Ca2+]i wave elicited by mechanical stimulation. The effect of protein phosphorylation was measured by modulating the protein kinase C (PKC), protein kinase A (PKA), and tyrosine kinase activity.METHODS:
Cultured RPE cells isolated from neonatal control Long-Evans (LE) and dystrophic RCS rats were analyzed using the fluorescent dye fluo-3 to measure the Ca2+-wave propagation on mechanical stimulation to investigate the intercellular communication.RESULTS:
Mechanical stimulation in LE-RPE cells resulted in a centrifugally spreading Ca2+ wave through the neighboring cells. When a mechanical stimulus was applied on RCS-RPE cells, a significantly reduced Ca2+-response was found in the neighboring cells compared with that of control RPE cells. Activation of PKC almost completed blocked the mechanically induced Ca2+ rise in the neighboring RCS-RPE cells. In contrast to LE-RPE cells, an activation of PKA also significantly decreased the Ca2+-wave propagation in RCS-RPE cells. Inhibition of PKA had no effect on the intercellular communication in LE- or RCS-RPE cells. In addition, when protein phosphatase activity or tyrosine kinase activity was inhibited, an increased Ca2+ rise in the neighboring cells on mechanical stimulation was measured, reaching levels currently found for LE-RPE cells.CONCLUSIONS:
In dystrophic RCS-RPE cells, a decreased intercellular Ca2+-wave propagation is found. This intercellular communication can be mediated by protein phosphorylation.
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Base de dados:
MEDLINE
Assunto principal:
Epitélio Pigmentado Ocular
/
Degeneração Retiniana
/
Cálcio
Idioma:
En
Ano de publicação:
1998
Tipo de documento:
Article