ArticleThe Journal of clinical investigation1993
Disruption of cytoskeletal structures mediates shear stress-induced endothelin-1 gene expression in cultured porcine aortic endothelial cells.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 121 citations in OpenAlex.
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- Vascular mechanotransduction.Physiological reviews · 2023Review
- CFTR limits F-actin formation and promotes morphological alignment with flow in human lung microvascular endothelial cells.Physiological reports · 2021Article
- Editorial: Understanding molecular interactions that underpin vascular mechanobiology.APL bioengineering · 2021Article
- Specification of the mouse cardiac conduction system in the absence of Endothelin signaling.Developmental biology · 2014Article
- Single-cell imaging of mechanotransduction in endothelial cells.Progress in molecular biology and translational science · 2014Review
- Effects of shear stress cultivation on cell membrane disruption and intracellular calcium concentration in sonoporation of endothelial cells.Journal of biomechanics · 2011Article
- The role of cellular adaptation to mechanical forces in atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2008Review
- Crosstalk between endothelin and nitric oxide in the control of vascular tone.Heart failure reviews · 2001Review
- Flow (shear stress)-induced endothelium-dependent dilation is altered in mice lacking the gene encoding for dystrophin.Circulation · 2001Article
- Regulation of the endothelin system by shear stress in human endothelial cells.The Journal of physiology · 2000Article
- Tissue angiotensin II and endothelin-1 modulate differently the response to flow in mesenteric resistance arteries of normotensive and spontaneously hypertensive rats.British journal of pharmacology · 2000Article
- Impaired flow-induced dilation in mesenteric resistance arteries from mice lacking vimentin.The Journal of clinical investigation · 1997Article
- Reduction of renal mass is lethal in mice lacking vimentin. Role of endothelin-nitric oxide imbalance.The Journal of clinical investigation · 1997Article
- Shear stress induction of the tissue factor gene.The Journal of clinical investigation · 1997Article
- Mechanotransduction through the endothelial cytoskeleton: mediation of flow- but not agonist-induced EDRF release.British journal of pharmacology · 1996Article
- The cis-acting phorbol ester "12-O-tetradecanoylphorbol 13-acetate"-responsive element is involved in shear stress-induced monocyte chemotactic protein 1 gene expression.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Sickle erythrocytes, after sickling, regulate the expression of the endothelin-1 gene and protein in human endothelial cells in culture.The Journal of clinical investigation · 1995Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemodynamic shear stress alters the architecture and functions of vascular endothelial cells. We have previously shown that the synthesis of endothelin-1 (ET-1) in endothelial cells is increased by exposure to shear stress. Here we examined whether shear stress-induced alterations in cytoskeletal structures are responsible for increases in ET-1 synthesis in cultured porcine aortic endothelial cells. Exposure of endothelial cells to 5 dyn/cm2 of low shear stress rapidly increased monomeric G-actin contents within 5 min without changing total actin contents. The ratio of G- to total actin, 54 +/- 0.8% in quiescent endothelial cells, increased to 87 +/- 4.2% at 6 h and then decreased. Following the disruption of filamentous (F)-actin into G-actin, ET-1 mRNA levels in endothelial cells also increased within 30 min and reached a peak at 6 h. The F-actin stabilizer, phalloidin, abolished shear stress-induced increases in ET-1 mRNA; however, it failed to inhibit increases in ET-1 mRNA secondary to other stimulants. This indicates that shear stress-induced increases in ET-1 mRNA levels may be mediated by the disruption of actin fibers. Furthermore, increases in ET-1 gene expression can be induced by actin-disrupting agents, cytochalasin B and D. Another cytoskeleton-disrupting agent, colchicine, which inhibits dimerization of tubulin, did not affect the basal level of ET-1 mRNA. However, colchicine completely inhibited shear stress- and cytochalasin B-induced increases in ET-1 mRNA levels. These results suggest that shear stress-induced ET-1 gene expression in endothelial cells is mediated by the disruption of actin cytoskeleton and this induction is dependent on the integrity of microtubules.
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