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Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine

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Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine. / Brandner, Johanna M; Schulzke, Jörg D.

In: CELL TISSUE RES, Vol. 360, No. 3, 08.02.2015, p. 723-748.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Brandner, JM & Schulzke, JD 2015, 'Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine', CELL TISSUE RES, vol. 360, no. 3, pp. 723-748. https://doi.org/10.1007/s00441-014-2096-1

APA

Brandner, J. M., & Schulzke, J. D. (2015). Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine. CELL TISSUE RES, 360(3), 723-748. https://doi.org/10.1007/s00441-014-2096-1

Vancouver

Brandner JM, Schulzke JD. Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine. CELL TISSUE RES. 2015 Feb 8;360(3):723-748. https://doi.org/10.1007/s00441-014-2096-1

Bibtex

@article{f9231508726246bbaf5df9405adbfe12,
title = "Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine",
abstract = "The tight junction (TJ) regulates paracellular barrier properties. TJs are composed of transmembrane proteins, i.e., claudins, occludin, tricellulin and junctional adhesion molecules as well as TJ plaque proteins. Their relative abundance and composition determines epithelial tightness. TJs undergo rapid regulation by various signalling pathways, either directly addressing TJ transmembrane proteins or via plaque proteins and the cytoskeleton. In the skin, TJs exert predominantly barrier functions, while in the intestine they also mediate paracellular ion and water transport. In diseases, TJs can either be primarily affected (hereditary TJ defects) or changes can result from secondary regulatory inputs as, e.g., in inflammatory diseases (secondary TJ defects). Secondary TJ defects can maintain disease activity, e.g., by enhanced antigen leak. This review discusses TJ composition, function and regulation as well as primary and secondary tight junction defects in a comparative manner in skin and intestine in order to elucidate similarities and differences.",
author = "Brandner, {Johanna M} and Schulzke, {J{\"o}rg D}",
year = "2015",
month = feb,
day = "8",
doi = "10.1007/s00441-014-2096-1",
language = "English",
volume = "360",
pages = "723--748",
journal = "CELL TISSUE RES",
issn = "0302-766X",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine

AU - Brandner, Johanna M

AU - Schulzke, Jörg D

PY - 2015/2/8

Y1 - 2015/2/8

N2 - The tight junction (TJ) regulates paracellular barrier properties. TJs are composed of transmembrane proteins, i.e., claudins, occludin, tricellulin and junctional adhesion molecules as well as TJ plaque proteins. Their relative abundance and composition determines epithelial tightness. TJs undergo rapid regulation by various signalling pathways, either directly addressing TJ transmembrane proteins or via plaque proteins and the cytoskeleton. In the skin, TJs exert predominantly barrier functions, while in the intestine they also mediate paracellular ion and water transport. In diseases, TJs can either be primarily affected (hereditary TJ defects) or changes can result from secondary regulatory inputs as, e.g., in inflammatory diseases (secondary TJ defects). Secondary TJ defects can maintain disease activity, e.g., by enhanced antigen leak. This review discusses TJ composition, function and regulation as well as primary and secondary tight junction defects in a comparative manner in skin and intestine in order to elucidate similarities and differences.

AB - The tight junction (TJ) regulates paracellular barrier properties. TJs are composed of transmembrane proteins, i.e., claudins, occludin, tricellulin and junctional adhesion molecules as well as TJ plaque proteins. Their relative abundance and composition determines epithelial tightness. TJs undergo rapid regulation by various signalling pathways, either directly addressing TJ transmembrane proteins or via plaque proteins and the cytoskeleton. In the skin, TJs exert predominantly barrier functions, while in the intestine they also mediate paracellular ion and water transport. In diseases, TJs can either be primarily affected (hereditary TJ defects) or changes can result from secondary regulatory inputs as, e.g., in inflammatory diseases (secondary TJ defects). Secondary TJ defects can maintain disease activity, e.g., by enhanced antigen leak. This review discusses TJ composition, function and regulation as well as primary and secondary tight junction defects in a comparative manner in skin and intestine in order to elucidate similarities and differences.

U2 - 10.1007/s00441-014-2096-1

DO - 10.1007/s00441-014-2096-1

M3 - SCORING: Journal article

C2 - 25663273

VL - 360

SP - 723

EP - 748

JO - CELL TISSUE RES

JF - CELL TISSUE RES

SN - 0302-766X

IS - 3

ER -