Ca2+ SIGNALING IN INJURED IN SITU ENDOTHELIUM OF RAT AORTA

ROBERTO BERRA-ROMANI; ABDUL RAQEEB; JOSÉ EVERARDO AVELINO-CRUZ; FRANCESCO MOCCIA,; AMANDA OLDANI; FRANCISCO SPERONI; VANNI TAGLIETTI; FRANCO TANZI

CELL CALCIUM.

Elsevier

Año: 2008 vol. 44 p. 298 - 308

0143-4160

Summary The inner wall of excised rat aorta was scraped by a microelectrode and Ca2+ signalswere investigated by fluorescence microscopy in endothelial cells (ECs) directly coupled withinjured cells. The injury caused an immediate increase in the intracellular Ca2+ concentration([Ca2+]i), followed by a long-lasting decay phase due to Ca2+ influx from extracellular space.The immediate response was mainly due to activation of purinergic receptors, as shown by theeffect of P2X and P2Y receptors agonists and antagonists, such as suramin, ,-MeATP, MRS-2179and 2-MeSAMP. Inhibition of store-operated Ca2+ influx did not affect either the peak responseor the decay phase. Furthermore, the latter was: (i) insensitive to phospholipase C inhibition,(ii) sensitive to the gap junction blockers, palmitoleic acid, heptanol, octanol and oleamide,and (iii) sensitive to La3+ and Ni2+, but not to Gd3+. Finally, ethidium bromide or Lucifer Yellowdid not enter ECs facing the scraped area.These results suggest that endothelium scraping: (i) causes a short-lasting stimulation ofhealthy ECs by extracellular nucleotides released from damaged cells and (ii) uncouples thehemichannels of the ECs facing the injury site; these hemichannels do not fully close and allowa long-lasting Ca2+ entry.© 2007 Elsevier Ltd. All rights reserved.