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Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Mol+Cell+Biol 2016 ; 36 (7): 1124-35 Nephropedia Template TP
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Type I Interferons Control Proliferation and Function of the Intestinal Epithelium #MMPMID26811327
Katlinskaya YV; Katlinski KV; Lasri A; Li N; Beiting DP; Durham AC; Yang T; Pikarsky E; Lengner CJ; Johnson FB; Ben-Neriah Y; Fuchs SY
Mol Cell Biol 2016[Apr]; 36 (7): 1124-35 PMID26811327show ga
Wnt pathway-driven proliferation and renewal of the intestinal epithelium must be tightly controlled to prevent development of cancer and barrier dysfunction. Although type I interferons (IFN) produced in the gut under the influence of microbiota are known for their antiproliferative effects, the role of these cytokines in regulating intestinal epithelial cell renewal is largely unknown. Here we report a novel role for IFN in the context of intestinal knockout of casein kinase 1? (CK1?), which controls the ubiquitination and degradation of both ?-catenin and the IFNAR1 chain of the IFN receptor. Ablation of CK1? leads to the activation of both ?-catenin and IFN pathways and prevents the unlimited proliferation of intestinal epithelial cells despite constitutive ?-catenin activity. IFN signaling contributes to the activation of the p53 pathway and the appearance of apoptotic and senescence markers in the CK1?-deficient gut. Concurrent genetic ablation of CK1? and IFNAR1 leads to intestinal hyperplasia, robust attenuation of apoptosis, and rapid and lethal loss of barrier function. These data indicate that IFN play an important role in controlling the proliferation and function of the intestinal epithelium in the context of ?-catenin activation.