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17931663

Source:http://linkedlifedata.com/resource/pubmed/id/17931663

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pubmed-article:17931663pubmed:abstractTextIn order to determine whether integrin dynamics is associated with intracellular Ca(2+) concentration ([Ca(2+)](i)) mobilization in ECs in response to hemodynamic forces, changes in [Ca(2+)](i) in fluo-4-loaded cultured bovine aortic endothelial cells (BAECs) under fluid flow conditions were visualized employing laser scanning confocal microscopy. Following the onset of flow stimulus, transient increases in [Ca(2+)](i) occurred several times in individual BAECs during the 30-min observation period. The frequency of these [Ca(2+)](i) transients was clearly reduced by the application of an integrin antagonist (GRGDSP peptide). Furthermore, treatment of cells with an integrin activator (Mn(2+)) resulted in reduction of peak [Ca(2+)](i) levels and elevated frequency, which was markedly rescued upon GRGDSP administration. In contrast, an actin de-polymerizing agent (cytochalasin D) exerted no inhibitory effects; rather, cytochalasin D more likely facilitated [Ca(2+)](i) transients. Moreover, [Ca(2+)](i) transients, which were suppressed by short interference RNA-induced silencing of alphav integrin, exhibited greater frequently in cells cultured on vitronectin substratum in comparison with those cultured on fibronectin or collagen substratum. Either removal of extracellular Ca(2+), application of an inhibitor of endoplasmic reticulum Ca(2+)-ATPase (thapsigargin) or non-selective cation channel blocker (La(3+)) inhibited the [Ca(2+)](i) transients. Additionally, [Ca(2+)](i) transients were attenuated by extracellular signal-regulated kinase (ERK) kinase inhibitor (U0126); in contrast, [Ca(2+)](i) transients were unaffected by tyrosine kinase inhibitor (genistein) or phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002). Therefore, our findings revealed that alphav integrin dynamics modulates the frequency of flow-induced [Ca(2+)](i) transients in BAECs in an ERK-dependent fashion.lld:pubmed
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pubmed-article:17931663pubmed:authorpubmed-author:OhataHisayuki...lld:pubmed
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pubmed-article:17931663pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:17931663pubmed:articleTitleModulation of Ca2+ transients in cultured endothelial cells in response to fluid flow through alphav integrin.lld:pubmed
pubmed-article:17931663pubmed:affiliationDepartment of Pharmacology, School of Pharmaceutical Sciences, Showa University, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan. taku@pharm.showa-u.ac.jplld:pubmed
pubmed-article:17931663pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17931663pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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