کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4156012 1273764 2013 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
IGF-2 mediates intestinal mucosal hyperplasia in retinoblastoma protein (Rb)-deficient mice
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی پریناتولوژی (پزشکی مادر و جنین)، طب اطفال و بهداشت کودک
پیش نمایش صفحه اول مقاله
IGF-2 mediates intestinal mucosal hyperplasia in retinoblastoma protein (Rb)-deficient mice
چکیده انگلیسی

PurposeWe have previously demonstrated a hyperplastic phenotype when Rb expression was disrupted within the intestinal epithelium. These findings mimic resection-induced adaptation suggesting a possible mechanistic role for Rb during adaptation. The purpose of the present study was to elucidate a mechanism for how Rb deficiency induces intestinal hyperplasia.MethodsEnterocytes isolated from intestine-specific Rb knockout mice (Rb-IKO) underwent a microarray to elucidate their gene expression profile. IGF2 expression was significantly elevated, which was subsequently confirmed by RT-PCR and in situ mRNA hybridization. Mice with deficient expression of IGF2 or its receptor IGF1R were therefore crossed with Rb-IKO mice to determine the significance of IGF2 in mediating the Rb-IKO intestinal phenotype.ResultsExpression of IGF2 was significantly elevated in villus enterocytes of Rb-IKO mice. The mucosal hyperplasia in Rb-IKO mice was reversed when either IGF2 or IGF1R expression was genetically disrupted in Rb-IKO mice.ConclusionIGF-2 expression is significantly elevated in villus enterocytes and is required for the hyperplastic intestinal mucosal phenotype of Rb-IKO mice. The trophic effects of IGF2 require intact IGF1R signaling within the intestinal epithelium. These findings reveal novel regulatory roles for Rb in expanding intestinal mucosal surface area.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Pediatric Surgery - Volume 48, Issue 6, June 2013, Pages 1340–1347
نویسندگان
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