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Review
. 2008 Mar;1778(3):709-16.
doi: 10.1016/j.bbamem.2007.07.027. Epub 2007 Aug 24.

Stimulus-induced reorganization of tight junction structure: the role of membrane traffic

Dan Yu  1 , Jerrold R Turner
Affiliations
Review

Stimulus-induced reorganization of tight junction structure: the role of membrane traffic

Dan Yu et al. Biochim Biophys Acta. 2008 Mar.

Abstract

The tight junction forms a barrier that limits paracellular movement of water, ions, and macromolecules. The permeability properties of this barrier are regulated in response to both physiological and pathophysiological stimuli, and this regulation has been modeled by pharmacological agents. Although it is now known that vesicular traffic plays important roles in tight junction assembly, the molecular mechanisms by which vesicular traffic contributes to tight junction regulation remain to be defined. This review summarizes recent progress in understanding mechanisms and pathways of tight junction protein internalization and the relevance of these to tight junction regulation.

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Conflict of interest statement

No conflicts of interest exist.

Figures

Figure 1
Figure 1
Molecular composition of the tight junction. Tight junctions consist of three main groups of proteins. They are transmembrane proteins, e.g. claudins and occludin, cytoplasmic plaque proteins, e.g. ZO-1, ZO-2, ZO-3, and cingulin, and cytoskeletal and signaling proteins, e.g. actin, myosin II, and PKCζ. These proteins are interact to maintain tight junction structure.
Figure 2
Figure 2
Stimulus-induced endocytosis of tight junction proteins. Calcium depletion causes clathrin-mediated endocytosis of adherens junction (E-cadherin) and tight junction (claudin, occludin) proteins. TNF core family members caused caveolae-mediated endocytosis of occludin, but not other proteins. Both pathways involve actomyosin-dependent processes. The fate of these vesicles, including whether they fuse with lysosomes, resulting in protein degradation, or with recycling endosomes, with protein trafficking back to the tight junction, remains to be defined.
Figure 3
Figure 3
Occludin is internalized in vivo after immune activation. T cells were activated in vivo by intraperitoneal injection of anti-CD3 antibody. This resulted in TNF-dependent occludin (red) internalization. F-actin (green) and nuclei (blue) are shown for reference.
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