Regular ArticleA Defective EGF-Receptor inWaved-2Mice Attenuates Intestinal Adaptation☆
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Intestinal adaptation and rehabilitation
2023, Seminars in Pediatric SurgeryEpithelial PIK3R1 (p85) and TP53 Regulate Survivin Expression during Adaptation to Ileocecal Resection
2016, American Journal of PathologyThe Pathogenesis of Resection-Associated Intestinal Adaptation
2016, Cellular and Molecular Gastroenterology and HepatologyCitation Excerpt :Through several subsequent experimental paradigms, enhanced resection-induced adaptation responses have been verified after stimulation of the EGF receptor either by exogenous EGF,71,72 in EGF transgenic mice,73 or administration of another EGF-receptor ligand (transforming growth factor-α).74 Alternatively, inhibiting EGF-receptor signaling by removing the submandibular glands, a major source of endogenous EGF in the mouse,75 performing SBR procedures in waved-2 mice with diminished EGF-receptor activity,76 or administration of a pharmacologic EGF-receptor inhibitor77 all resulted in attenuated adaptation responses. Because the intestinal mucosa is a very dynamic organ containing some of the most rapidly proliferating cells in the body, the relationship between rates of cell production and cell death must be precise.
Mechanisms of intestinal adaptation
2016, Best Practice and Research: Clinical GastroenterologyBoth epidermal growth factor and insulin-like growth factor receptors are dispensable for structural intestinal adaptation
2015, Journal of Pediatric SurgeryCitation Excerpt :Alternatively, it must be considered that EGFR and IGF1R signaling functions to regulate adaptation within the underlying submucosal and muscularis compartments of the intestine. Previously, we have observed resection-induced adaptation when intestinal epithelial EGFR was selectively deleted [13], but not when EGFR was globally inhibited [11,38]. Regarding IGF1R, it is plausible that the IGF system stimulates adaptation via non-epithelial cells within the intestine.
The role of growth factors in intestinal regeneration and repair in necrotizing enterocolitis
2013, Seminars in Pediatric Surgery
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This research was supported by a Trustee's Grant from the Children's Hospital Research Foundation, Children's Hospital Medical Center, Cincinnati, OH (B.W.W., recipient).
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To whom correspondence and reprint requests should be addressed at Division of Pediatric Surgery, Children's Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH 45229-3039. Fax: (513) 559-7657; E-mail: [email protected].