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E-GEOD-68984 - The transferrin receptor is required for intestinal epithelial homeostasis
Released on 19 May 2015, last updated on 24 May 2015
The role of Tfr1 in non-erythroid tissues remains elusive due to the embryonic lethality of the Tfr1 global knockout mouse model. To bypass this problem, we generated a mouse model in which Tfr1 was conditionally deleted in intestinal epithelial cells (IECs). These mice developed severe IEC disruption, characterized by blunted villi, edema, loss of proliferative intervillus IECs, accumulation of lipids, and early neonatal lethality. Strikingly, a wide range of genes associated with epithelial-to-mesenchymal transition were highly upregulated in IEC lacking Tfr1. Additionally, candidate vesicular transport and sorting genes implicated in lipid absorption and trafficking were downregulated. Surprisingly, the presence of a mutant allele of Tfr1, which is unable to bind to iron-loaded transferrin, was capable of rescuing the lethality, intestinal epithelial homeostasis, and proliferation in a majority of the Tfr1 conditional knockout mice. 9 samples (3 wildtype, 3 knockout, 3 rescue) were prepared from the intestinal epithelial cells isolated from the small intestine and proximal colon.
transcription profiling by array
Nancy C Andrews <email@example.com>, Alan Chen