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Vasoactive amines modulate actin cables (stress fibers) and surface area in cultured bovine endothelium
Journal article   Peer reviewed

Vasoactive amines modulate actin cables (stress fibers) and surface area in cultured bovine endothelium

Seth L Welles, David Shepro and Herbert B Hechtman
Journal of cellular physiology, v 123(3), pp 337-342
Jun 1985
PMID: 4039330

Abstract

Cultured bovine aortic endothelial cells were fixed and stained with NBD‐phallicidin and quantitated with a digital image analyzer for changes in actin cables and surface area. Serotonin (5‐HT), norepinephrine (NE), dopamine and histamine (all at 10−4M concentrations) were tested for their ability to induce cytoskeletal changes. Only 5‐HT and NE increased action cables significantly (p < 0.01), 80.7% and 97.9%, respectively. Dopamine and histamine treated cells showed a 67.4% and 80.8% decrease in actin cables respectively (p < 0.01). Stimulated increases of actin cables by 5‐HT were inhibited by Ketanserin, and propranoiol inhibited NE stimulation of actin cables. Treatment of cells with these blockers alone also decreased actin cables below control values (p < 0.01). Pretreatment of cells with diphenhydramine, but not cimetidine, inhibited histamine‐induced decreases in actin cables. Stimulation of surface area by 5‐HT and NE was also observed, with 40.8% and 80.7% increases respectively, when compared with controls (p < 0.01). The increases in actin cables were associated with a lack of ruffled edges that are indicative of motile cells. In contrast, induced decreases in actin cables resulted in cells with ruffled edges. Exogenous 5‐HT and NE have been shown to prevent the increased permeability visible as extravasation of red blood cells from postcapillary venules in thrombocytopenic animals. The present data suggest that 5‐HT and NE may be involved in maintaining the endothelial barrier function by a receptor‐mediated stimulation of actin cables. Also, histamine‐induced decreases in actin cables may be correlated with the amine's action in vivo as a mediator of increased inflammatory permeability.

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
Physiology
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