In vivo induction of tight junction proliferation in rat liver.

Montesano, Roberto; Gabbiani, G.; Perrelet, Alain; Orci, Lelio

doi:10.1083/jcb.68.3.793

Cited by 83 publications

(28 citation statements)

References 13 publications

(12 reference statements)

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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: 71%

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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Section: Discussionmentioning

confidence: 71%

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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“…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)(8)(9) and an extensive rearrangement of hepatocyte junctional elements observed by freeze-fracture electron microscopy (10).…”

mentioning

confidence: 99%

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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“…The shortest center-to-center distance between adjacent granules measured 90 to 100 A. Montesano et al 1975Montesano et al , 1976 .…”

Section: And Discussionmentioning

confidence: 99%

The occurrence of electron dense intercellular materials and gap junctions in the human intestinal epithelium.

Sano

Konno

Igarashi

et al. 1977

Tohoku J. Exp. Med.

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In vivo induction of tight junction proliferation in rat liver.

Cited by 83 publications

References 13 publications

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

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

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

The occurrence of electron dense intercellular materials and gap junctions in the human intestinal epithelium.

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