ArticlePflugers Archiv : European journal of physiology1994
Cytoskeletal modulation of the response to mechanical stimulation in human vascular endothelial cells.
Article in Pflugers Archiv : European journal of physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 48 citations in OpenAlex.
- Identification of key signaling molecules involved in the activation of the swelling-activated chloride current in human glioblastoma cells.The Journal of membrane biology · 2014Article
- The role of cellular adaptation to mechanical forces in atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2008Review
- Hypotonic activation of volume-sensitive outwardly rectifying anion channels (VSOACs) requires coordinated remodeling of subcortical and perinuclear actin filaments.The Journal of membrane biology · 2005Article
- Absence of dystrophin in mice reduces NO-dependent vascular function and vascular density: total recovery after a treatment with the aminoglycoside gentamicin.Arteriosclerosis, thrombosis, and vascular biology · 2004Article
- Involvement of Rho-kinase and tyrosine kinase in hypotonic stress-induced ATP release in bovine aortic endothelial cells.The Journal of physiology · 2001Article
- Flow (shear stress)-induced endothelium-dependent dilation is altered in mice lacking the gene encoding for dystrophin.Circulation · 2001Article
- Reduced intracellular ionic strength as the initial trigger for activation of endothelial volume-regulated anion channels.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Role of Rho and Rho kinase in the activation of volume-regulated anion channels in bovine endothelial cells.The Journal of physiology · 1999Article
- Lysophosphatidic acid stimulates neurotransmitter-like conductance changes that precede GABA and L-glutamate in early, presumptive cortical neuroblasts.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Impaired flow-induced dilation in mesenteric resistance arteries from mice lacking vimentin.The Journal of clinical investigation · 1997Article
- Modulation of inwardly rectifying potassium channels in cultured bovine pulmonary artery endothelial cells.The Journal of physiology · 1997Article
- Mechanotransduction through the endothelial cytoskeleton: mediation of flow- but not agonist-induced EDRF release.British journal of pharmacology · 1996Article
- The volume-activated chloride current in endothelial cells from bovine pulmonary artery is not modulated by phosphorylation.Pflugers Archiv : European journal of physiology · 1996Article
- Modulation of a volume-regulated chloride current by F-actin.The Journal of membrane biology · 1995Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Possible interactions of cytoskeletal elements with mechanically induced membrane currents and Ca2+ signals were studied in human endothelial cells by using a combined patch-clamp and Fura II technique. For mechanical stimulation, cells were exposed to hypotonic solution (HTS). The concomitant cell swelling activates a Cl- current, releases Ca2+ from intracellular stores and activates Ca2+ influx. To interfere with the cytoskeleton, cells were loaded either with the F-actin-stabilizing agent phalloidin (10 mumol/l), or the F-actin-depolymerizing substance cytochalasin B (50 mumol/l). These were administered either in the bath or the pipette solutions. The tubulin structure of the endothelial cells was modulated by taxol (50 mumol/l), which supports polymerization of tubulin, or by the depolymerizing agent colcemid (10 mumol/l) both applied to the bath. Immunofluorescence experiments show that under the chosen experimental conditions the cytoskeletal modifiers employed disintegrate the F-actin and microtubuli cytoskeleton. Neither of these cytoskeletal modifiers influenced the HTS-induced Cl- current. Ca2+ release was not affected by cytochalasin B, taxol or colcemid, but was suppressed if the cells were loaded with phalloidin. Depletion of intracellular Ca2+ stores by thapsigargin renders the intracellular [Ca2+] sensitive to the extracellular [Ca2+], which is indicative of a Ca2+ entry pathway activated by store depletion. Neither cytochalasin B nor phalloidin affected this Ca2+ entry. We conclude that F-actin turnover or depolymerization is necessary for Ca2+ release by mechanical activation. The tubulin network is not involved. The Ca2+ release- activated Ca2+ entry is not modulated by the F-actin cytoskeleton.
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