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Altered distribution of tight junction proteins after intestinal ischaemia/reperfusion injury in rats.

Authors: Li, Q  Zhang, Q  Wang, C  Liu, X  Qu, L  Gu, L  Li, N  Li, J 
Citation: Li Q, etal., J Cell Mol Med. 2009 Sep;13(9B):4061-76. Epub 2009 Nov 19.
Pubmed: (View Article at PubMed) PMID:19929946
DOI: Full-text: DOI:10.1111/j.1582-4934.2009.00975.x

Tight junction (TJ) disruptions have been demonstrated both in vitro and more recently in vivo in infection. However, the molecular basis for changes of TJ during ischaemia-reperfusion (I/R) injury is poorly understood. In the present study, intestinal damage was induced by I/R in an animal model. As assessed by TUNEL and propidium iodide uptake, we showed that I/R injury induced apoptosis as well as necrosis in rat colon, and the frequency of apoptotic and necrotic cells reached the maximum at 5 hrs of reperfusion. Immunofluorescence microscopy revealed that claudins 1, 3 and 5 are strongly expressed in the surface epithelial cells of the colon; however, labelling of all three proteins was present diffusely within cells and no longer focused at the lateral cell boundaries after I/R. Using Western blot analysis, we found that distribution of TJ proteins in membrane microdomains of TJ was markedly affected in I/R injury rats. Occludin, ZO-1, claudin-1 and claudin-3 were completely displaced from TX-100 insoluble fractions to TX-100 soluble fractions, and claudin-5 was partly displaced. The distribution of lipid raft marker protein caveolin-1 was also changed after I/R. I/R injury results in the disruption of TJs, which characterized by relocalization of the claudins 1, 3 and 5 and an increase in intestinal permeability using molecular tracer measurement. I/R injury altered distribution of TJ proteins in vivo that was associated with functional TJ deficiencies.


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RGD Object Information
RGD ID: 2325127
Created: 2010-05-20
Species: All species
Last Modified: 2010-05-20
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.