Epidermal growth factor is critical for intestinal adaptation following small bowel resection

Stern, Lawrence E.; Erwin, Christopher R.; O’Brien, David; Huang, Frederick S.; Warner, Brad W.

doi:10.1002/1097-0029(20001015)51:2<138::aid-jemt5>3.0.co;2-t

Cited by 58 publications

(19 citation statements)

References 35 publications

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“…EGFR has been shown to be of crucial importance for postresectional intestinal adaptation [31,[42][43][44]. Stimulation of EGFR in vivo was found to result in an enhancement, whereas its' inhibition led to attenuation of post-resectional intestinal adaptation [42]. Also, intestinal adaptation was found to be markedly impaired in waved-two mice (who have a hypofunctional EGFR signalling) [43].…”

Section: Discussionmentioning

confidence: 99%

Intestinal epithelial cell proliferation is dependent on the site of massive small bowel resection

et al. 2007

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Early intestinal adaptation after massive small bowel resection (SBR) is driven by increased epithelial cell (EC) proliferation. There is a clear clinical difference in the post-operative course of patients after the loss of proximal (P) compared to distal (D) small bowel. This study examined the effects of the site of SBR on post-resectional intestinal adaptation, and investigated the potential mechanisms involved. C57BL/6J mice (n = 7/group) underwent: (1) 60% P-SBR, (2) 60% D-SBR, (3) 60% mid (M)-SBR and (4) SHAM-operation (transection/reanastomosis). Mice were sacrificed at 7 days after surgery and ECs and adjacent mucosal lymphocytes (IELs) isolated. Adaptation was assessed in both jejunum and ileum by quantification of villus height, crypt depth, villus cell size, crypt cell size (microns), goblet cell number, and EC proliferation (%BrdU incorporation). Proliferation signalling pathways including keratinocyte growth factor (KGF)/KGFR(1), IL-7/IL-7R, and epidermal growth factor receptor (EGFR) were measured by RT-PCR. Expression of IL-7 was further analysed by immunofluorescence. Data were analyzed using ANOVA. All three SBR models led to significant increases in villus height, crypt depth, goblet cell numbers and EC proliferation rate when compared to respective SHAM groups. The strongest morphometric changes were found for jejunal segments after M-SBR and for ileal segments after P-SBR. Furthermore, morphometric analysis showed that at 1-week post-resection a tremendous increase in EC numbers occurred in jejunal villi (cell hyperplasia), whereas a significant increase in EC size predominated in ileal villi (cell hypertrophy). mRNA expression of KGF, KGFR(1), IL-7R, and EGFR showed a significant increase only after D-SBR, whereas IL-7 increased significantly after SBR in all investigated models, and this was confirmed by immunofluorescence studies. Early intestinal adaptation shows distinct differences depending on the site of SBR, and is predominately driven by cell hyperplasia in jejunal villi and cell hypertrophy in ileal villi. However, the exact mechanisms, which guide these signalling pathways are still unclear.

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Section: Discussionmentioning

confidence: 99%

Intestinal epithelial cell proliferation is dependent on the site of massive small bowel resection

et al. 2007

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“…1-3 A number of growth factors and nutrients may help to mediate these changes. 1,[4][5][6][7] In addition to an increase in functional absorption, adaptation also consists of an increase in villus length and crypt depth, and an increased number of microvilli. This adaptation requires a remodeling of the crypt-villus complex and includes significant increases in both epithelial cell (EC) proliferation as well as EC apoptosis.…”

Section: Introductionmentioning

confidence: 99%

“…11 A number of local and distant trophic factors contribute to this adaptation. 5,[12][13][14][15] Intraepithelial lymphocytes (IEL) also have a role in this adaptive process. The gamma delta T-cell receptor sub-population of the IEL, as an example, express the trophic molecule keratinocyte growth factor (KGF), which is up-regulated during intestinal mucosal injury, 16 and following massive small bowel resection.…”

Section: Introductionmentioning

confidence: 99%

Intestinal intraepithelial lymphocyte derived angiotensin converting enzyme modulates epithelial cell apoptosis

et al. 2005

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“…It has demonstrated that the important physiological defensive system of intestine consists of the normal intestinal bacterial ecology, expellant movement of intestine, chemical protection of peptic juice, mucosal barrier, and distinctive immune system. It had been found that some members in the growth factor family, such as epithelial growth factor and fibroblast growth factor, can promote growth and maturation of intestinal mucosal epithelium, 31,32 and some proinflammatory cytokines can also modulate the barrier function. 33,34 Ingredients of food, such as glutamine and some special fibers, are important for sustaining the integrity of mucosa.…”

Section: Discussionmentioning

confidence: 99%

Regulatory Effect of Histamine on the Barrier Function of Intestinal Mucosal

Duan

Chen

Alexander

2010

Journal of Gastrointestinal Surgery

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Epidermal growth factor is critical for intestinal adaptation following small bowel resection

Cited by 58 publications

References 35 publications

Intestinal epithelial cell proliferation is dependent on the site of massive small bowel resection

Intestinal epithelial cell proliferation is dependent on the site of massive small bowel resection

Intestinal intraepithelial lymphocyte derived angiotensin converting enzyme modulates epithelial cell apoptosis

Regulatory Effect of Histamine on the Barrier Function of Intestinal Mucosal

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