Cell kinetics in flat (avillous) mucosa of the human small intestine

Wright, Nicholas A.; Watson, Alexander; Morley, A. R.; Appleton, David R.; Marks, Janet

doi:10.1136/gut.14.9.701

Cited by 124 publications

(39 citation statements)

References 17 publications

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“…Furthermore, we demonstrated that the number of enteroblasts per 100/~m crypt length is not influenced by the treatment, and concluded that hyperplasia is the predominant mechanism for the enlargement of this compartment. A similar transformation of the crypt region is observed in coeliac disease [28] and in the experimental blind loop syndrome [21], both situations also being characterized by increased proliferation. Thus, it seems likely that a three-dimensional increase in crypt size and a concomitant decrease in the number of crypts per unit serosal area is a specific feature when cell production rate is altered in this way.…”

Section: Discussionmentioning

confidence: 61%

Three-dimensional structure and cell kinetics at different sites of rat intestinal remnants during the early adaptive response to resection

et al. 1982

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In this study the early phase of the morphological adaptation of rat ileum after a proximal resection of 60% has been studied using microdissection and cell labelling techniques. Resected rats and sham-operated controls were killed 2, 4, 6, 10 and 12 days after surgery. Intraperitoneal injections of 3H-thymidine were carried out 24 or 12 h prior to sacrifice. In the latter groups mitotic arrest was achieved by vincristine. A stereo-microscope was used to measure and calculate the following parameters: intestinal diameter; villus: height, width, breadth at base and apex, surface, enterocytes per 100 micrometers length, cell pool, number of villi and absorptive surface per mm2 serosal area; crypt: length, enteroblasts per 100 micrometers length and per column, cell columns and mitoses per crypt, cell pool, crypts, and mitoses per unit serosal area; cell kinetics: migration rate, villus transit time. To test the influence of treatments, postoperative time course and the location of the intestinal segment and their possible interactions, factorial analyses of variance were carried out on the parameters investigated. The main findings, demonstrated for the first time, were: 1. An increase in the villus surface which was achieved by proportional enlargement of villus geometry; 2. This increase in the villus surface led to an enlarged absorptive surface per unit serosal area; 3. A reduction of villus transit time of the individual enterocyte; 4. A most pronounced magnitude of adaptative response in the proximal remnants which was gradually diminished in aboral direction, and 5. A sequential course of adaptative response of the various crypt parameters investigated.

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Section: Discussionmentioning

confidence: 61%

Three-dimensional structure and cell kinetics at different sites of rat intestinal remnants during the early adaptive response to resection

et al. 1982

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“…l5 For estimation of the size of the proliferative compartment (PC) a graphical method was used, determining the 50% peak value of the mitotic index distribution curve. 16 sectioned crypts and cells per circumference of 150 cross sectioned crypts. At the time of death, blood was sampled for gastrin radioimmunoassay.…”

Section: Cell Proliferation Studiesmentioning

confidence: 99%

Chronic ethanol consumption selectively stimulates rectal cell proliferation in the rat.

Simanowski¹,

Seitz²,

Baier³

et al. 1986

Gut

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“…Generally, gut inflammatory reactions to bacterial pathogens and parasites in the colon lead to increased epithelial proliferation [31,32]. Celiac disease is the classical bowel disease associated with increased epithelial proliferation, where the pathology involves a Th1/IFN-g response to gluten and massively increased cell proliferation in the crypts of Lieberkühn of the upper small bowel [33,34]. Therefore, the statement in the paper under evaluation that "Prolonged intestinal inflammation inhibits IEC (intestinal epithelial cell) proliferation and promotes cell death" is not generally sustainable.…”

Section: Discussionmentioning

confidence: 99%

Cytokine regulation of intestinal epithelial cell proliferation

MacDonald¹

2010

Expert Review of Clinical Immunology

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Evaluation of: Nava P, Koch S, Laukoetter MG et al. Interferon-g regulates intestinal epithelial homeostasis through converging b-catenin signaling pathways. Immunity 32(3), 392-402 (2010).Inflammation in the gut is associated with changes in the epithelial layer. Barrier function is diminished, epithelial cell death may occur and the epithelial cells themselves secrete proinflammatory cytokines. One of the most obvious changes, however, is in the rate of epithelial renewal, which most often manifests as increased epithelial proliferation, with an increase in mucosal thickness in the colon and the length of the crypts of Lieberkühn in the small bowel. The factors that control the basal rate of renewal and the epithelial stem cell niche have been well studied and it is clear that Wnt signaling is critically important. Inflammatory cytokines, therefore, may alter epithelial renewal in the gut by modifying or antagonizing Wnt signaling pathways.

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Cell kinetics in flat (avillous) mucosa of the human small intestine

Cited by 124 publications

References 17 publications

Three-dimensional structure and cell kinetics at different sites of rat intestinal remnants during the early adaptive response to resection

Three-dimensional structure and cell kinetics at different sites of rat intestinal remnants during the early adaptive response to resection

Chronic ethanol consumption selectively stimulates rectal cell proliferation in the rat.

Cytokine regulation of intestinal epithelial cell proliferation

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