Background/aims: Knockdown of protein tyrosine phosphatase nonreceptor type 2 () exaggerates IFN-γ-induced intestinal barrier defects, but mice constitutively lacking in epithelial cells (PTPN2xVilCre mice) do not show changes in epithelial function or enhanced susceptibility to experimental colitis. Here, we investigated whether PTPN2 modulates the expression of related tyrosine phosphatases.
Methods: PTPN2 knockdown in HT-29 cells was induced using siRNA constructs. Acute colitis in PTPN2xVilCre mice was induced by 2% dextran sulfate sodium (DSS) in drinking water for 7 days. Colitis-associated tumors were induced by injection of azoxymethane prior to treatment with DSS for 3 consecutive cycles.
Results: In HT-29 cells, depletion resulted in enhanced mRNA expression of and and in parallel to upregulation of mRNA upon treatment with TNF for 24 h. DSS treatment of PTPN2-deficient mice resulted in a strong induction of mRNA in colon tissue in vivo. In the tumor model, mRNA was again clearly upregulated in nontumor tissue from PTPN2-deficient mice; however, this was not observed in tumor tissue.
Conclusions: Our experiments show that PTPN23 function might, at least partially, compensate lack of PTPN2 in epithelial cells. Upregulation of PTPN23 might therefore crucially contribute to the lack of a colitis phenotype in PTPN2-VilCre mice.
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| http://dx.doi.org/10.1159/000499157 | DOI Listing |
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