Formation of intestinal atresias in the Fgfr2IIIb-/- mice is not associated with defects in notochord development or alterations in Shh expression.

The Journal of Surgical Research
Amy L ReederPeter F Nichol

Abstract

The etiology of intestinal atresia remains elusive but has been ascribed to a number of possible events including in utero vascular accidents, failure of recanalization of the intestinal lumen, and mechanical compression. Another such event that has been postulated to be a cause in atresia formation is disruption in notochord development. This hypothesis arose from clinical observations of notochord abnormalities in patients with intestinal atresias as well as abnormal notochord development observed in a pharmacologic animal model of intestinal atresia. Atresias in this model result from in utero exposure to Adriamycin, wherein notochord defects were noted in up to 80% of embryos that manifested intestinal atresias. Embryos with notochord abnormalities were observed to have ectopic expression of Sonic Hedgehog (Shh), which in turn was postulated to be causative in atresia formation. We were interested in determining whether disruptions in notochord development or Shh expression occurred in an established genetic model of intestinal atresia and used the fibroblast growth factor receptor 2IIIb homozygous mutant (Fgfr2IIIb-/-) mouse model. These embryos develop colonic atresias (100% penetrance) and duodenal atresias (42% penetran...Continue Reading

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Citations

Jan 8, 2014·The Journal of Surgical Research·Amy L ReederPeter F Nichol
Dec 24, 2013·The Journal of Surgical Research·Krzysztof M ZarembaPeter F Nichol
Apr 1, 2017·Disability and Rehabilitation. Assistive Technology·João Pedro ProençaPedro Vieira
Mar 27, 2020·Frontiers in Pharmacology·Matthew L M JonesWarwick J Teague
Apr 23, 2020·International Journal of Molecular Medicine·Antonios KostourosJohn Tsiaoussis

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