Intracellular Ca2+ stores are essential for injury induced Ca2+ signaling and re-endothelialization

✍ Scribed by Zhiqiang Zhao; Petr Walczysko; Min Zhao

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 694 KB
• Volume: 214
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.21248

✦ Synopsis

Abstract

Endothelialization repairs the lining of damaged vasculature and is a key process in preventing thrombosis and restenosis. It has been demonstrated that extracellular calcium ([Ca^2+^]~o~) influx is important for subsequent endothelialization. The role of intracellular Ca^2+^ stores in mechanical denudation induced intracellular calcium ([Ca^2+^]~i~) rise and endothelialization remains to be demonstrated. Using monolayer culture of a human endothelial cell line (human umbilical vein endothelial cell, HUVEC), we investigated [Ca^2+^]~i~ wave propagation and re‐endothelialization following mechanical denudation. Consistent with previous reports for other types of cells, mechanical denudation induces calcium influx, which is essential for [Ca^2+^]~i~ rise and endothelialization. Moreover, we found that intracellular Ca^2+^ stores are also essential for denudation induced [Ca^2+^]~i~ wave initiation and propagation, and the subsequent endothelialization. Thapsigargin which depletes intracellular Ca^2+^ stores completely abolished [Ca^2+^]~i~ wave generation and endothelialization. Xestospongin C (XeC), which prevents Ca^2+^ release from intracellular Ca^2+^ stores by inhibition of inositol 1,4,5‐trisphosphate (IP~3~) receptor, inhibited intercellular Ca^2+^ wave generation and endothelialization following denudation. Purinergic signaling through a suramin sensitive mechanism and gap junction communication also contribute to in intercellular Ca^2+^ wave propagation and re‐endothelialization. We conclude that intracellular Ca^2+^ stores, in addition to extracellular Ca^2+^, are essential for intracellular Ca^2+^ signaling and subsequent endothelialization following mechanical denudation. J. Cell. Physiol. 214: 595–603, 2008. © 2007 Wiley‐Liss, Inc.