Ca(2+) is a highly versatile second messenger that plays a key role in the regulation of many cell processes. This versatility resides in the fact that different signals can be encoded spatio-temporally by varying the frequency and amplitude of the Ca(2+) response. A typical example of an organized
Microfilament and microtubule assembly is required for the propagation of inositol trisphosphate receptor-induced Ca2+ waves in bovine aortic endothelial cells
✍ Scribed by Éric Béliveau; Gaétan Guillemette
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 562 KB
- Volume
- 106
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
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.
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