Expressions of E-cadherin, pl20ctn, p-catenin and NF-KB in Ulcerative Colitis
This study was aimed to investigate the expressions of E-cadherin, p120 ctn, β-catenin and NF-κB in ulcerative colitis(UC) tissues and the implications of their expressions in the pathogenesis of UC. The expressions of E-cadherin, p120 ctn, β-catenin and NF-κB were detected by immunohistochemistry,...
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Veröffentlicht in: | 华中科技大学学报:医学英德文版 2015, Vol.35 (3), p.368-373 |
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Sprache: | eng |
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Zusammenfassung: | This study was aimed to investigate the expressions of E-cadherin, p120 ctn, β-catenin and NF-κB in ulcerative colitis(UC) tissues and the implications of their expressions in the pathogenesis of UC. The expressions of E-cadherin, p120 ctn, β-catenin and NF-κB were detected by immunohistochemistry, and those of p120 ctn and NF-κB by Western blotting in 23 cases of UC and 17 cases of normal colonic tissues. The relationship between the expression of E-cadherin or NF-κB and that of p120 ctn was analyzed by Spearman rank correlation analysis. The results showed that in UC and normal colonic groups, the abnormal expression rate of E-cadherin, p120 ctn, β-catenin, and NF-κB was 52.2% vs. 0(P〈0.05), 73.9% vs. 23.5%(P〈0.05), 65.2% vs. 17.6%(P〈0.05) and 78.4% vs. 23.5%(P〈0.05), respectively. p120 ctn expression was positively correlated with E-cadherin expression(r=0.404, P〈0.05), but negatively with nuclear NF-κB expression(r= – 0.347, P〈0.05). Western blotting showed that as compared with the normal controls, the p120 ctn protein level was significantly decreased(P〈0.05), whereas the NF-κB protein level was increased(P〈0.05) in UC tissues. It was concluded that in the colonic tissues of UC patients, the expressions of E-cadherin, p120 ctn and β-catenin are decreased, suggesting the mucosal barrier is impaired in UC. Moreover, NF-κB is increased and activated in the UC tissues, resulting in the inflammation in UC. p120 ctn may influence the UC development through modulating intercellular adhesion and inflammatory response. |
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ISSN: | 1672-0733 1993-1352 |