Intracellular Calcium, Endothelial Cells and Angiogenesis
Most mitogens, including angiogenic factors, generate cytosolic calcium rises through two mechanisms: entry from extracellular medium, through the opening of calcium permeable channels in the plasma membrane, or release from intracellular organelles (mainly endoplasmic reticulum, ER).
Calcium entry, the main topic of this review, can be dependent on previously IP3-activated emptying of calcium stores (store-dependent or capacitative calcium entry - CCE), or independent on it (non capacitative calcium entry, NCCE). The intracellular pathways underlying calcium entry are under investigation and recently arachidonic acid (AA) and nitric oxide (NO) metabolism have been suggested to play a key role, at least in some cell types. Even if some calcium entry blockers are under clinical trial with encouraging results, a better knowledge about the molecular nature of calcium channels and their intracellular regulation, together with a more detailed description of spatiotemporal dynamics of intracellular calcium events, could lead to new and more specific strategies in therapeutical approach to cancer progression and angiogenesis.
Document Type: Research Article
Affiliations: Department of Animal and Human Biology, University of Torino and Nanostructured Interfaces and Surfaces Centre of Excellence (NIS), Via Accademia Albertina 13, 10123 Torino, Italy.
Publication date: 2006-01-01
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