title: A decreased Ca2+-wave propagation is found among cultured RPE cells from dystrophic RCS rats.
abstract: OBJECTIVE
  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.
authors.affiliation: Laboratory of Physiology, KU Leuven, Belgium.
authors.forename: P
authors.initials: P
authors.lastname: Stalmans
authors.forename: B
authors.initials: B
authors.lastname: Himpens
mesh_terms: D000814:Aniline Compounds / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D002450:Cell Communication / Q000502:physiology; D002478:Cells, Cultured; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005456:Fluorescent Dyes / Q000378:metabolism; D019319:Okadaic Acid / Q000494:pharmacology; D010766:Phosphorylation; D010857:Pigment Epithelium of Eye / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D051381:Rats; D011922:Rats, Mutant Strains; D012162:Retinal Degeneration / Q000378:metabolism*; D013314:Stress, Mechanical; D019284:Thapsigargin / Q000494:pharmacology; D014966:Xanthenes / Q000378:metabolism
chemical_list: D000814:Aniline Compounds; D004791:Enzyme Inhibitors; D005456:Fluorescent Dyes; D014966:Xanthenes; D019319:Okadaic Acid; C059715:Fluo-3; D019284:Thapsigargin; D011505:Protein-Tyrosine Kinases; D017346:Protein Serine-Threonine Kinases; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D000252:Calcium-Transporting ATPases; D002118:Calcium