Opposite Regulation of Transepithelial Electrical Resistance and Paracellular Permeability by Rho in Madin-Darby Canine Kidney Cells

Hasegawa, Hiroshi; Fujita, Hirotada; Katoh, Hironori; Aoki, Jun; Nakamura, Kazuhiro; Ichikawa, Atsushi; Negishi, Manabu

doi:10.1074/jbc.274.30.20982

Cited by 62 publications

(60 citation statements)

References 58 publications

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“…Several lines of evidence from cell and organ culture experiments suggest that RhoA participates in diverse aspects of epithelial development, such as tubulogenesis, cyst formation, epithelial barrier function and epithelial polarity (Bruewer et al, 2004;Eisen et al, 2006;Hasegawa et al, 1999;Meyer et al, 2006;Micheal et al, 2005;Rosário and Birchmeier, 2003). Consistent with the above, blockade of the RhoA effector ROCK, via Y27632, in developing kidneys is associated with a diverse set of phenotypic changes, and ROCK has been implicated in several distinct steps during kidney development (Meyer et al, 2006;Michael et al, 2005).…”

Section: Research Articlesupporting

confidence: 49%

“…Consistent with previous studies (Michael et al, 2005;Meyer et al, 2006), we observed that a higher degree of ROCK blockade led to rapid structural deformities in the entire developing metanephros, including swelling and increased lumen in ureteric tips. The latter may be associated with a loss of epithelial barrier function, which has previously been suggested to be regulated by Rho GTPases (Fujita et al, 2000;Hasegawa et al, 1999). Interestingly, Sema4d was observed to partially rescue some of these structural anamolies, either via an increase in RhoA activity and the consequential drop in the degree of ROCK blockade, or through the actions of other signalling mediators activated downstream of plexin B1.…”

Section: Research Articlementioning

confidence: 89%

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A functional role for semaphorin 4D/plexin B1 interactions in epithelial branching morphogenesis during organogenesis

et al. 2008

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Semaphorins and their receptors, plexins, carry out important functions during development and disease. In contrast to the wellcharacterized plexin A family, however, very little is known about the functional relevance of B-type plexins in organogenesis, particularly outside the nervous system. Here, we demonstrate that plexin B1 and its ligand Sema4d are selectively expressed in epithelial and mesenchymal compartments during key steps in the genesis of some organs. This selective expression suggests a role in epithelial-mesenchymal interactions. Importantly, using the developing metanephros as a model system, we have observed that endogenously expressed and exogenously supplemented Sema4d inhibits branching morphogenesis during early stages of development of the ureteric collecting duct system. Our results further suggest that the RhoA-ROCK pathway, which is activated downstream of plexin B1, mediates these inhibitory morphogenetic effects of Sema4d and suppresses branch-promoting signalling effectors of the plexin B1 signalling complex. Finally, mice that lack plexin B1 show early anomalies in kidney development in vivo. These results identify a novel function for plexin B1 as a negative regulator of branching morphogenesis during kidney development, and suggest that the Sema4d-plexin B1 ligand-receptor pair contributes to epithelial-mesenchymal interactions during organogenesis via modulation of RhoA signalling.

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Section: Research Articlesupporting

confidence: 49%

Section: Research Articlementioning

confidence: 89%

A functional role for semaphorin 4D/plexin B1 interactions in epithelial branching morphogenesis during organogenesis

et al. 2008

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“…Activation of Rho has been linked to regulation of tight junction structure and function (44)(45)(46)(47). Overexpression of constitutively active or dominant-negative RhoA results in striking morphological alterations, such as a loss of the normal tight junction strand morphology (48), whereas Rho activation in MDCK cells results in a selective increase in paracellular permeability of low-molecular-weight tracers (49). It is likely that receptor subtype distribution between cells as well as variations in tight junctions regulation by Rho through effectors like ROCKI varies among lung cells (44,47,(49)(50)(51)(52).…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: S1P ₃ receptor-induced reorganization of epithelial tight junctions compromises lung barrier integrity and is potentiated by TNF

Gon

Wood²,

Kiosses³

et al. 2005

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

124

118

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Pulmonary pathologies including adult respiratory distress syndrome are characterized by disruption of pulmonary integrity and edema compromising respiratory function. Sphingosine 1-phosphate (S1P) is a lipid mediator synthesized and/or stored in mast cells, platelets, and epithelial cells, with production up-regulated by the proinflammatory cytokines IL-1 and TNF. S1P administration via the airways but not via the vasculature induces lung leakage. Using receptor-null mice, we show that S1P, acting on S1P3 receptor expressed on both type I and type II alveolar epithelial cells but not vascular endothelium, induces pulmonary edema by acute tight junction opening. WT but not S1P3-null mice showed disruption of pulmonary epithelial tight junctions and the appearance of paracellular gaps between epithelial cells by electron microscopy within 1 h of airways exposure to S1P. We further show by fluorescence microscopy that S1P induced rapid loss of ZO-1 reactivity, an essential component of the cytoplasmic plaque associated with tight junctions, as well as of the tetraspannin Claudin-18, an integral membrane organizer of tight junctions. S1P shows synergistic activity with the proinflammatory cytokine TNF, showing both pulmonary edema and mortality at subthreshold S1P doses. Specifically, preexposure of mice to subthreshold doses of TNF, which alone induced no lung edema, exacerbated S1P-induced edema and impaired survival. S1P, acting through S1P3, regulates epithelial integrity and acts additively with TNF in compromising respiratory barrier function. Because S1P3-null mice are resistant to S1P-induced pulmonary leakage, either alone or in the presence of TNF, S1P3 antagonism may be useful in protecting epithelial integrity in pulmonary disease

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“…Human Rac1 was obtained as described previously (18). cDNA for Ha-Ras was obtained from Health Science Research Resources Bank (Osaka, Japan).…”

Section: Methodsmentioning

confidence: 99%

Differential Responses to Nerve Growth Factor and Epidermal Growth Factor in Neurite Outgrowth of PC12 Cells Are Determined by Rac1 Activation Systems

Yasui

Katoh

Yamaguchi

et al. 2001

Journal of Biological Chemistry

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Opposite Regulation of Transepithelial Electrical Resistance and Paracellular Permeability by Rho in Madin-Darby Canine Kidney Cells

Cited by 62 publications

References 58 publications

A functional role for semaphorin 4D/plexin B1 interactions in epithelial branching morphogenesis during organogenesis

A functional role for semaphorin 4D/plexin B1 interactions in epithelial branching morphogenesis during organogenesis

RETRACTED: S1P ₃ receptor-induced reorganization of epithelial tight junctions compromises lung barrier integrity and is potentiated by TNF

Differential Responses to Nerve Growth Factor and Epidermal Growth Factor in Neurite Outgrowth of PC12 Cells Are Determined by Rac1 Activation Systems

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Opposite Regulation of Transepithelial Electrical Resistance and Paracellular Permeability by Rho in Madin-Darby Canine Kidney Cells

Cited by 62 publications

References 58 publications

A functional role for semaphorin 4D/plexin B1 interactions in epithelial branching morphogenesis during organogenesis

A functional role for semaphorin 4D/plexin B1 interactions in epithelial branching morphogenesis during organogenesis

RETRACTED: S1P 3 receptor-induced reorganization of epithelial tight junctions compromises lung barrier integrity and is potentiated by TNF

Differential Responses to Nerve Growth Factor and Epidermal Growth Factor in Neurite Outgrowth of PC12 Cells Are Determined by Rac1 Activation Systems

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Product

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RETRACTED: S1P ₃ receptor-induced reorganization of epithelial tight junctions compromises lung barrier integrity and is potentiated by TNF