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Bves Modulates Tight Junction Associated Signaling

Blood vessel epicardial substance (Bves) is a transmembrane adhesion protein that regulates tight junction (TJ) formation in a variety of epithelia. The role of TJs within epithelium extends beyond the mechanical properties. They have been shown to play a direct role in regulation of RhoA and ZONAB/...

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Autores principales: Russ, Patricia K., Pino, Christopher J., Williams, Christopher S., Bader, David M., Haselton, Frederick R., Chang, Min S.
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024319/
https://www.ncbi.nlm.nih.gov/pubmed/21283798
http://dx.doi.org/10.1371/journal.pone.0014563
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author Russ, Patricia K.
Pino, Christopher J.
Williams, Christopher S.
Bader, David M.
Haselton, Frederick R.
Chang, Min S.
author_facet Russ, Patricia K.
Pino, Christopher J.
Williams, Christopher S.
Bader, David M.
Haselton, Frederick R.
Chang, Min S.
author_sort Russ, Patricia K.
collection PubMed
description Blood vessel epicardial substance (Bves) is a transmembrane adhesion protein that regulates tight junction (TJ) formation in a variety of epithelia. The role of TJs within epithelium extends beyond the mechanical properties. They have been shown to play a direct role in regulation of RhoA and ZONAB/DbpA, a y-box transcription factor. We hypothesize that Bves can modulate RhoA activation and ZONAB/DbpA activity through its regulatory effect on TJ formation. Immortalized human corneal epithelial (HCE) cells were stably transfected with Flag-tagged full length chicken Bves (w-Bves) or C-terminus truncated Bves (t-Bves). We found that stably transfected w-Bves and t-Bves were interacting with endogenous human Bves. However, interaction with t-Bves appeared to disrupt cell membrane localization of endogenous Bves and interaction with ZO-1. w-Bves cells exhibited increased TJ function reflected by increased trans-epithelial electrical resistance, while t-Bves cells lost TJ protein immunolocalization at cell-cell contacts and exhibited decreased trans-epithelial electrical resistance. In parental HCE and w-Bves cells ZONAB/DbpA and GEF-H1 were seen at cell borders in the same pattern as ZO-1. However, expression of t-Bves led to decreased membrane localization of both ZONAB/DbpA and GEF-H1. t-Bves cells had increased RhoA activity, as indicated by a significant 30% increase in FRET activity compared to parental HCE cells. ZONAB/DbpA transcriptional activity, assessed using a luciferase reporter probe, was increased in t-Bves cells. These studies demonstrate that Bves expression and localization can regulate RhoA and ZONAB/DbpA activity.
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spelling pubmed-30243192011-01-31 Bves Modulates Tight Junction Associated Signaling Russ, Patricia K. Pino, Christopher J. Williams, Christopher S. Bader, David M. Haselton, Frederick R. Chang, Min S. PLoS One Research Article Blood vessel epicardial substance (Bves) is a transmembrane adhesion protein that regulates tight junction (TJ) formation in a variety of epithelia. The role of TJs within epithelium extends beyond the mechanical properties. They have been shown to play a direct role in regulation of RhoA and ZONAB/DbpA, a y-box transcription factor. We hypothesize that Bves can modulate RhoA activation and ZONAB/DbpA activity through its regulatory effect on TJ formation. Immortalized human corneal epithelial (HCE) cells were stably transfected with Flag-tagged full length chicken Bves (w-Bves) or C-terminus truncated Bves (t-Bves). We found that stably transfected w-Bves and t-Bves were interacting with endogenous human Bves. However, interaction with t-Bves appeared to disrupt cell membrane localization of endogenous Bves and interaction with ZO-1. w-Bves cells exhibited increased TJ function reflected by increased trans-epithelial electrical resistance, while t-Bves cells lost TJ protein immunolocalization at cell-cell contacts and exhibited decreased trans-epithelial electrical resistance. In parental HCE and w-Bves cells ZONAB/DbpA and GEF-H1 were seen at cell borders in the same pattern as ZO-1. However, expression of t-Bves led to decreased membrane localization of both ZONAB/DbpA and GEF-H1. t-Bves cells had increased RhoA activity, as indicated by a significant 30% increase in FRET activity compared to parental HCE cells. ZONAB/DbpA transcriptional activity, assessed using a luciferase reporter probe, was increased in t-Bves cells. These studies demonstrate that Bves expression and localization can regulate RhoA and ZONAB/DbpA activity. Public Library of Science 2011-01-20 /pmc/articles/PMC3024319/ /pubmed/21283798 http://dx.doi.org/10.1371/journal.pone.0014563 Text en Russ et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Russ, Patricia K.
Pino, Christopher J.
Williams, Christopher S.
Bader, David M.
Haselton, Frederick R.
Chang, Min S.
Bves Modulates Tight Junction Associated Signaling
title Bves Modulates Tight Junction Associated Signaling
title_full Bves Modulates Tight Junction Associated Signaling
title_fullStr Bves Modulates Tight Junction Associated Signaling
title_full_unstemmed Bves Modulates Tight Junction Associated Signaling
title_short Bves Modulates Tight Junction Associated Signaling
title_sort bves modulates tight junction associated signaling
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024319/
https://www.ncbi.nlm.nih.gov/pubmed/21283798
http://dx.doi.org/10.1371/journal.pone.0014563
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