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Microfilament and microtubule assembly is required for the propagation of inositol trisphosphate receptor‐induced Ca 2+ waves in bovine aortic endothelial cells
Author(s) -
Béliveau Éric,
Guillemette Gaétan
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22011
Subject(s) - microbiology and biotechnology , caveolae , microtubule , microfilament , endoplasmic reticulum , second messenger system , cytoskeleton , biology , inositol , actin , intracellular , receptor , chemistry , biophysics , signal transduction , cell , biochemistry
Ca 2+ is a highly versatile second messenger that plays a key role in the regulation of numerous cell processes. One‐way cells ensure the specificity and reliability of Ca 2+ signals is by organizing them spatially in the form of waves that propagate throughout the cell or within a specific subcellular region. In non‐excitable cells, the inositol 1,4,5‐trisphosphate receptor (IP 3 R) is responsible for the release of Ca 2+ from the endoplasmic reticulum. The spatial aspect of the Ca 2+ signal depends on the organization of various elements of the Ca 2+ signaling toolkit and varies from tissue to tissue. Ca 2+ is implicated in many of endothelium functions that thus depend on the versatility of Ca 2+ signaling. In the present study, we showed that the disruption of caveolae microdomains in bovine aortic endothelial cells (BAEC) with methyl‐ß‐cyclodextrin was not sufficient to disorganize the propagation of Ca 2+ waves when the cells were stimulated with ATP or bradykinin. However, disorganizing microfilaments with latrunculin B and microtubules with colchicine both prevented the formation of Ca 2+ waves. These results suggest that the organization of the Ca 2+ waves mediated by IP 3 R channels does not depend on the integrity of caveolae in BAEC, but that microtubule and microfilament cytoskeleton assembly is crucial. J. Cell. Biochem. 106: 344–352, 2009. © 2008 Wiley‐Liss, Inc.