Effect of plant cytokinins on microfilaments and tight junction permeability

Bentzel, Carl J.; Hainau, Bo; Edelman, A.; Anagnostopoulos, T.; Benedetti, E.L.

doi:10.1038/264666a0

Cited by 83 publications

(34 citation statements)

References 6 publications

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“…Thus, it is likely that the shift in equilibrium from G-to F-actin in the hepatocyte had effects on transport functions that were not measured in the present study but might well influence bile formation. However, the changes in junctional structure and permeability were of particular interest because there is suggestive evidence in epithelial tissues that microfilaments can influence the permeability of junctional complexes (25), and the present findings are consistent with this interpretation.…”

Section: Discussionsupporting

confidence: 81%

Phalloidin-induced cholestasis: a microfilament-mediated change in junctional complex permeability.

Elias¹,

Hruban²,

Wade³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

104

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Phalloidin, administered to male rats for 7 days (500 ,sg per kg/day), increased the mean hepatic content of filamentous actin. Both bile flow and bile acid excretion diminished proportionally, whereas the bile-to-plasma ratios of Phalloidin, a cyclic peptide derived from the poisonous mushroom Amanita phalloides, specifically binds to purified muscle F-actin and prevents its depolymerization (1-3). Phalloidin increases the quantity of F-actin when added to isolated hepatocytes (4) or to isolated liver plasma membranes (2, 5, 6) and produces a marked increase in microfilaments in the pericanalicular region of hepatocytes when the alkaloid is administered chronically in low doses to rats (7). In the intact rat, chronic phalloidin administration, like other microfilament poisons, is associated with a diminution in bile production (7-9) and an extensive rearrangement of hepatocyte junctional elements observed by freeze-fracture electron microscopy (10).These changes in junctional structure suggest that microfilaments help regulate junctional development and support the notion that the junctional barrier may in turn influence the formation of bile. Because accumulating evidence suggests that the paracellular pathway is an important site for water, electrolyte, and solute entry into bile (11-14), the phalloidin-treated rat provides a useful experimental model to examine more closely the relationship among microfilament function, junctional structure, and bile secretion. In this study, we measure the effects of phalloidin on bile formation and biliary permeability to inulin and sucrose, two large molecular weight solutes that rapidly reach equilibrium between plasma and bile before liver water, suggesting that their entry into bile is via a paracellular route. Junctional structure and permeability were also examined by freezefracture studies and by the infusion of ionic lanthanum chloride at a time when increases in hepatic content of polymerized actin were also observed. METHODSMale Sprague-Dawley rats (Charles River), initially weighing 175-225 g, were treated for 7 days with either phalloidin at 500 ug kg-' day-' in saline (16 animals) or saline alone as a control (16 animals) by intraperitoneal injection as described by Gabbiani et al. (7). Phalloidin was obtained from Boehringer Mannheim. On the eighth day, the rats were anesthetized by intraperitoneal injection of sodium phenobarbital at 50 mg (kg of body weight)-I, and the bile duct was cannulated with polyethylene tubing (PE10, Clay Adams). Body temperature was monitored by rectal probe and maintained at 370C by a heating lamp regulated by a constant temperature regulator (Yellow Springs Instrument). After 60-80 min, the abdomen was reopened and heparin (10,000 units kg-') was injected into the inferior vena cava before fixation of the liver by portal vein perfusion.Bile Flow and Bile Acid Excretion. Bile was collected for 80 min at 20-min intervals and expressed as !ul mind (g of body weight)-l and as gl min-1 (g of liver)-l. Bile acids were analyzed ...

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Section: Discussionsupporting

confidence: 81%

Phalloidin-induced cholestasis: a microfilament-mediated change in junctional complex permeability.

Elias¹,

Hruban²,

Wade³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

104

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“…Various actin disrupting drugs such as cytokinins, phalloidin, and cytochalasins disturb TJ structure and permeability (9,31,38). We observed that CytoD induced significant discontinuity of ZO-1 immunoreactivity (Fig.…”

Section: Discussionmentioning

confidence: 72%

A transmural pressure gradient induces mechanical and biological adaptive responses in endothelial cells

DeMaio

Tarbell

Scaduto³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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A sudden increase in the transmural pressure gradient across endothelial monolayers reduces hydraulic conductivity (Lp), a phenomenon known as the sealing effect. To further characterize this endothelial adaptive response, we measured bovine aortic endothelial cell (BAEC) permeability to albumin and 70-kDa dextran, Lp, and the solvent-drag reflection coefficients () during the sealing process. The diffusional permeability coefficients for albumin (1.33 Ϯ 0.18 ϫ 10 Ϫ6 cm/s) and dextran (0.60 Ϯ 0.16 ϫ 10 Ϫ6 cm/s) were measured before pressure application. The effective permeabilities (measured when solvent drag contributes to solute transport) of albumin and dextran (P e alb and P e dex ) were measured after the application of a 10 cmH2O pressure gradient; during the first 2 h of pressure application, P e alb , P e dex , and Lp were significantly reduced by 2.0 Ϯ 0.3-, 2.1 Ϯ 0.3-, and 3.7 Ϯ 0.3-fold, respectively. Immunostaining of the tight junction (TJ) protein zonula occludens-1 (ZO-1) was significantly increased at cell-cell contacts after the application of transmural pressure. Cytochalasin D treatment significantly elevated transport but did not inhibit the adaptive response, whereas colchicine treatment had no effect on diffusive permeability but inhibited the adaptive response. Neither cytoskeletal inhibitor altered despite significantly elevating both Lp and effective permeability. Our data suggest that BAECs actively adapt to elevated transmural pressure by mobilizing ZO-1 to intercellular junctions via microtubules. A mechanical (passive) component of the sealing effect appears to reduce the size of a small pore system that allows the transport of water but not dextran or albumin. Furthermore, the structures of the TJ determine transport rates but do not define the selectivity of the monolayer to solutes (). permeability; hydraulic conductivity; reflection coefficient; zonula occludens-1 THERE ARE TWO PRINCIPAL MECHANISMS of paracellular transport across the endothelium: bulk fluid movement or convection, a process driven by hydrostatic and oncotic pressure gradients, and diffusional exchange, a nonconvective process driven by concentration gradients (24, 42). These transport processes are characterized by three transport coefficients that define the barrier properties of the endothelium to water and solutes: hydraulic conductivity (L p ), diffusional permeability (P d ; i.e., when convection is zero), and the solvent-drag reflection coefficient (). The effective permeability (P e ; measured when solvent drag contributes to solute flux) is also reported frequently in the literature. It is conventional to regard the endothelial transport coefficients as constants; in other words, any observed change in transendothelial flux is attributed to changes in pressure and/or concentration gradients across the endothelium. However, it has become increasingly evident in recent years that endothelial transport coefficients also depend on the mechanical and hormonal environment of the cell layer.The endothelial cell...

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“…Several lines of evidence suggest an association between ZO-1 and actin filaments. Passage of ions and small molecules through the TJ is regulated by epithelial cells [Madara, 19881, and substantial data indicate that actin filament integrity is critical to this regulation [Bentzel et al, 1976;Montesano et al, 1976;Meza et al, 1980;Madara et al, 19861. ImmunoEM studies demonstrate that ZO-1 is clustered at the cytoplasmic surface of TJ membrane contact sites [Stevenson et al, 19881, the same points at which actin filaments appear to make contact with the membrane [Madara, 1987;Drenckhahn and Dermietzel, 19881.…”

Section: Discussionmentioning

confidence: 99%

Molecular environment of ZO‐1 in epithelial and non‐epithelial cells

Howarth

Stevenson

1995

Cell Motil. Cytoskeleton

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We previously reported the expression of ZO-1 in cell types that do not form tight junctions. Here we compare the molecular environments of ZO-1 in epithelial cells, primary cultures of astrocytes and in the non-epithelial S180 sarcoma cell line. ZO-1 co-localizes with a subset of actin filaments in all cell types. In astrocytes, ZO-1 is found concentrated in discrete bands at points of cell-cell contact. Indirect immunofluorescent microscopy shows that these bands of ZO-1 co-localize with the adherens junction proteins vinculin and alpha-actinin, and with the antigen recognized by a pan-cadherin antibody. In contrast, ZO-1 in S180 cells, which exhibit limited cell-cell interactions, is diffusely distributed over the plasma membrane, with concentrations in lamellipodia where actin filaments accumulate. ZO-1 does not co-localize with vinculin at focal adhesions in this cell type. Analysis of ZO-1 immunoprecipitation profiles from different cell types, performed under conditions previously demonstrated to maintain interactions between ZO-1, ZO-2 and p130 from the MDCK epithelial cell line, show that the proteins which co-precipitate with ZO-1 vary with cell type. Precipitation of polypeptides at 165 kDa, potentially ZO-2, and 65 kDa occurs in both a mouse kidney tubule epithelial cell line and the non-epithelial S180 cells. No proteins specifically associate with ZO-1 immunoprecipitated from astrocytes. Spectrin, alpha-actinin, vinculin and cadherin are not detected in immunoblots of ZO-1 immunoprecipitates from any cell type.

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Effect of plant cytokinins on microfilaments and tight junction permeability

Cited by 83 publications

References 6 publications

Phalloidin-induced cholestasis: a microfilament-mediated change in junctional complex permeability.

Phalloidin-induced cholestasis: a microfilament-mediated change in junctional complex permeability.

A transmural pressure gradient induces mechanical and biological adaptive responses in endothelial cells

Molecular environment of ZO‐1 in epithelial and non‐epithelial cells

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