Volume 13, Issue 9b pp. 4061-4076

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

Qiurong Li

Qiurong Li

Institute of General Surgery, Jinling Hospital, Nanjing, China

School of Medicine, Nanjing University, Nanjing, China

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Qiang Zhang

Qiang Zhang

Institute of General Surgery, Jinling Hospital, Nanjing, China

School of Medicine, Nanjing University, Nanjing, China

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Chenyang Wang

Chenyang Wang

Institute of General Surgery, Jinling Hospital, Nanjing, China

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Xiaoxiang Liu

Xiaoxiang Liu

National Key Laboratory of Crop Genetics and Germplasm Enhancement, Nanjing Agricultural University, Nanjing, China

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Linlin Qu

Linlin Qu

Institute of General Surgery, Jinling Hospital, Nanjing, China

School of Medicine, Nanjing University, Nanjing, China

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Lili Gu

Lili Gu

Institute of General Surgery, Jinling Hospital, Nanjing, China

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Ning Li

Ning Li

Institute of General Surgery, Jinling Hospital, Nanjing, China

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Jieshou Li

Corresponding Author

Jieshou Li

Institute of General Surgery, Jinling Hospital, Nanjing, China

Correspondence to: Jieshou LI, Institute of General Surgery, Jinling Hospital, No. 305 East Zhongshan Road, Nanjing 210002, China.
Tel.: 86-25-80860064
Fax: 86-25-84803956
E-mail: [email protected]Search for more papers by this author
First published: 29 January 2010
Citations: 39

The authors declare no conflict of interest.

Abstract

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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