Cytoskeletal reorganizations in human umbilical vein endothelial cells as a result of cytokine exposure

Molony, Leslie; Armstrong, Lydia

doi:10.1016/0014-4827(91)90454-3

Cited by 51 publications

(21 citation statements)

References 22 publications

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“…The fact that microtubules are subject to constant remodeling, because of the dynamic instability of tubulin dimers, prompted us to consider that the microtubule network may be an important actor in the transmission of activation signals inside the cell. This idea is supported by reports showing that: (i) microtubule reorganization, occurring during differentiation of HL 60 cells, is associated to tubulin phosphorylation on tyrosine residues (7); (ii) microtubule reorganization were also observed after cytokines and phorbol ester treatment of human umbilical vein endothelial cells (8); and (iii) microtubule disruption generates a signal that leads to NFB activation (9).…”

supporting

confidence: 53%

Microtubule Integrity Regulates Src-like and Extracellular Signal-regulated Kinase Activities in Human Pro-monocytic Cells

Schmid-Alliana¹,

Menou²,

Manié³

et al. 1998

Journal of Biological Chemistry

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(1993) J. Biol. Chem. 268, 13675-13681). Here, we provide evidence that disruption of the microtubule structure rapidly triggers extracellular signal-regulated kinase (ERK) activation, whereas it was without effect on SAPK2 activity, which is commonly acknowledged to control pro-inflammatory cytokine production. This process involves the activation of the entire cascade including Ras, Raf-1, MEK1/2, ERK1, and ERK2. Activation of ERKs is followed by their nuclear translocation. Although other SAPK congeners might be activated upon microtubule depolymerization, the activation of ERK1 and ERK2 is mandatory for IL-1 production as shown by the blocking effect of PD 98059, a specific MEK1/2 inhibitor. Additionally, we provide evidence that microtubule disruption also induces the activation of c-Src and Hck activities. The importance of Src kinases in the mediation of the colchicine effect is underscored by the fact that CP 118556, a specific inhibitor of Src-like kinase, abrogates both the colchicine-induced ERK activation and IL-1 production. This is the first evidence that ERK activation is an absolute prerequisite for induction of this cytokine. Altogether, our data lend support to a model where the status of microtubule integrity controls the level of Src activities that subsequently activate the ERK kinase cascade, thus leading to IL-1 production.

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supporting

confidence: 53%

Microtubule Integrity Regulates Src-like and Extracellular Signal-regulated Kinase Activities in Human Pro-monocytic Cells

Schmid-Alliana¹,

Menou²,

Manié³

et al. 1998

Journal of Biological Chemistry

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“…Some reports have implicated TGF-b1 in the induction of changes in endothelial cell phenotype, including loss of cell-cell contact, rearrangement in endothelial cell actin cytoskeleton and impairment of endothelial permeability (Coomber, 1991;Molony & Armstrong, 1991;Hurst et al, 1999;Goldberg et al, 2002). In this study, a fluorescence microscopy approach was used to analyse changes in actin distribution in HUVECs treated with TGF-b1 for 4 h. Although the presence of stress fibre-bearing cells was observed under all conditions, the quantification of at least five high-power fields showed that TGF-b1 treatment increased the number of endothelial cells exhibiting abundant stress fibre cells (37.5±4.3 % in treated cultures compared to the 12.45±2.4 % observed in untreated cells; Fig.…”

Section: Tgf-b1 Alters Microfilament Cytoskeleton Organization In Endmentioning

confidence: 99%

TGF-β1 induces transendothelial migration of the pathogenic fungus Sporothrix schenckii by a paracellular route involving extracellular matrix proteins

et al. 2007

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Sporotrichosis, a mycosis caused by Sporothrix schenckii, is characterized by lymphocutaneous lesions. In immunocompromised hosts, this fungus may invade the bloodstream and disseminate to other tissues, such as lung and bone. Our group previously showed that S. schenckii yeasts adhere to endothelial monolayers and that this interaction is modulated by cytokines. Using 3.0 mm-pore culture inserts, the present work shows that transforming growth factor (TGF)-b1 led to a 80±26 % increase in fungal migration across endothelial monolayers and inhibited fungus internalization by 55±23.5 %, when compared to untreated cells. The major surface endothelial molecules recognized by S. schenckii were not modulated by TGF-b1. These data suggested that a paracellular route is preferentially used by S. schenckii during the transmigration of cultured endothelial cells. It was further observed that TGF-b1 increased the subendothelial matrix exposure and that anti-fibronectin (anti-FN) and anti-laminin (anti-LM) antibodies abolished the increase in S. schenckii association with endothelial monolayers induced by TGF-b1. These antibodies also inhibited (38.2±4.29 % and 50.8±17.3 %, respectively) the adhesion of S. schenckii to freshly prepared native endothelial matrices. Furthermore, transendothelial migration of S. schenckii was blocked by anti-FN and anti-LM antibodies. These data indicate that TGF-b1-induced S. schenckii adhesion to endothelial monolayers results from the increased exposure of the subendothelial extracellular matrix and that this event may contribute to the enhancement of transendothelial migration.

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“…It has been reported that cancer cells induce morphological changes of mesothelial cells by releasing some unknown substances (Kimura et al, 1985;Uchiyama et al, 1992) and may damage the mesothelial cells by attachment onto the mesothelial surface (Kiyasu et al, 1981). In cultured endothelial cells, several substances, including thrombin (Laposata et al, 1983), active oxygen (Shasby et al, 1985), 12(S)-HETE (Tang et al, 1993), tumour necrosis factor, interferon-y, interleukin 1 (Molony and Armstrong, 1991), histamine (Carson et al, 1989) and tyrosine phosphatase inhibitor (Staddon et al, 1995), are confirmed to increase permeability. We did not find any noticeable signs of mesothelial cell damage by cancer cells in this study, but found that the medium conditioned by SST-2 cells rapidly and reversibly reduced TER across the mesothelial monolayer and caused the disappearance of 7H6 antigen from the cell border (data not shown).…”

Section: Ter Measurementsmentioning

confidence: 99%

Enhanced paracellular barrier function of rat mesothelial cells partially protects against cancer cell penetration

Tobioka

Sawada²,

Zhong³

et al. 1996

Br J Cancer

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Cytoskeletal reorganizations in human umbilical vein endothelial cells as a result of cytokine exposure

Cited by 51 publications

References 22 publications

Microtubule Integrity Regulates Src-like and Extracellular Signal-regulated Kinase Activities in Human Pro-monocytic Cells

Microtubule Integrity Regulates Src-like and Extracellular Signal-regulated Kinase Activities in Human Pro-monocytic Cells

TGF-β1 induces transendothelial migration of the pathogenic fungus Sporothrix schenckii by a paracellular route involving extracellular matrix proteins

Enhanced paracellular barrier function of rat mesothelial cells partially protects against cancer cell penetration

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