Cell proliferation studies in the intestinal epithelium of the rat I. Determination of the kinetic parameters

Cairnie, A. B.; Lamerton, L. F.; Steel, G. Gordon

doi:10.1016/0014-4827(65)90055-8

Cited by 344 publications

(119 citation statements)

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“…In the sections of jejunum, the "left" sides of 30 axially sectioned crypts wAere analysed per animal. The cell positions of labelled nuclei and of metaphase mitotic figures were recorded in terms of serial position counting upwards from Position 1 in the base of the crypt, together with the heights of individual crypts in cells (Cairnie, Lamerton and Steel, 1965); a cell was regarded as labelled if 5 or more grains were located over the nucleus (Wright, 1971). In each animal the data were projected on to a standard crypt the height of which was the mean crypt height of the animal concerned.…”

Section: Methodsmentioning

confidence: 99%

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Kinetics of changes in the crypts of the jejunal mucosa of dimethylhydrazine-treated rats

Sunter¹,

Appleton²,

Wright³

et al. 1978

Br J Cancer

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Summary.-When symmetrical 1,2 dimethylhydrazine was administered to rats by weekly s.c. injection, 37% of the animals had developed small intestinal carcinomas after 21-27 weeks. These lesions were largely localized to duodenum and upper jejunum. At the same time there was a diffuse crypt hyperplasia in the jejunum which affected all the treated animals, not just those with neoplasms. This marked hyperplasia was preceded by a modest sustained crypt elongation which was seen soon after DMH injections began.In these hyperplastic jejunal crypts the absolute size of the proliferative compartment was increased, but the growth fraction calculated from labelling studies appeared to fall, probably by reduction in relative size of the proliferating population within the proliferative compartment.No convincing alteration in actual cell-cycle time was observed in the abnormal crypts. There was a slight (25%) increase in cell-production rate in the abnormal crypts.

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Section: Methodsmentioning

confidence: 99%

“…By constructing cumulative-birth-rate curves a measure of the cell velocity at the top of the crypt can be obtained (Cairnie et al, 1965). A method has been described by WTright et al (1972).…”

Section: -16mentioning

confidence: 99%

Kinetics of changes in the crypts of the jejunal mucosa of dimethylhydrazine-treated rats

Sunter¹,

Appleton²,

Wright³

et al. 1978

Br J Cancer

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“…After birth, continuous proliferation of epithelial cells occurs only in the lower regions of the crypts (4,5), and cells migrate from there onto and along the villi, eventually being extruded from the tips into the lumen of the intestine. In adult rats and mice the generation time for the crypt cells is 10-14 hr (6), and the transit time along the length of the villus is approximately 48 hr (7). The characteristics of proliferation and migration of enterocytes in adult animals are dealt with in detail in the review by Lipkin (8).…”

Section: Morphologic Development Of the Intestinementioning

confidence: 99%

Biochemistry of Intestinal Development

Henning¹

1979

Environmental Health Perspectives

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In biochemical terms, the rat small intestine is relatively immature at birth and for the first two postnatal weeks. Then during the third week a dramatic array ofenzymic changes begins, and by the end ofthe fourth week the intestine has the digestive and absorptive properties of the adult. Selective examples of these changes are discussed with emphasis on their implications for toxicological studies. The review also includes a detailed consideration of the roles of the dietary change of weaning and of glucocorticoid and thyroid hormones in the regulation of intestinal development.My aim in this paper is to use the rat as a model system for a discussion of the postnatal development of small intestinal function. Factors which affect the developmental process will be reviewed in terms of their implications for toxicological studies. Morphologic Development of the IntestineBy the time of birth, the intestinal mucosa of the rat displays a high level of structural development characterized by villi lined with a single layer of columnar epithelial cells which have well-defined microvilli at their absorptive surface (1-3). After birth, continuous proliferation of epithelial cells occurs only in the lower regions of the crypts (4, 5), and cells migrate from there onto and along the villi, eventually being extruded from the tips into the lumen of the intestine. In adult rats and mice the generation time for the crypt cells is 10-14 hr (6), and the transit time along the length of the villus is approximately 48 hr (7). The characteristics of proliferation and migration of enterocytes in adult animals are dealt with in detail in the review by Lipkin (8). In neonatal rats, generation and migration of the cells is much slower than in adults. Despite the fact that the neonatal villi are shorter, the transit time is at least % hr (7, 9). During the third postnatal week there are significant changes in both cell kinetics and mor-

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“…Intestinal epithelial cells are among the most rapidly proliferating cells in the adult mammal, and it has been estimated that the epithelial mucosa of the gut is completely replaced every 3 ± 8 days (Cairnie et al, 1965;Cheng and Leblond, 1974). Renewal of the intestinal epithelium is a complex process.…”

Section: Introductionmentioning

confidence: 99%

TGF-β1 effects on proliferation of rat intestinal epithelial cells are due to inhibition of cyclin D1 expression

Sakai

et al. 1998

Oncogene

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Transforming growth factor-beta 1 (TGF-b1) arrests intestinal epithelial cells (RIE-1 and IEC-6) in the G1 phase of the cell cycle and inhibits cyclin D1 expression. This report describes experiments designed to elucidate the mechanism of cyclin D1 inhibition and to determine whether inhibition of cyclin D1 expression is the cause, rather than the result, of TGF-b1-mediated cell cycle arrest. TGF-b1 inhibition of IEC-6 cell proliferation was associated with a decrease in the abundance of cyclin D1/Cdk4 complexes and a corresponding decrease in Cdk4-dependent phosphorylation of the retinoblastoma protein. Metabolic labeling studies indicated that TGFb1 inhibited cyclin D1 synthesis without altering the rate of cyclin D1 protein degradation. Cyclin D1 antisense oligonucleotides blocked serum-stimulated induction of cyclin D1 and DNA synthesis, whereas cyclin D1 sense oligonucleotides had no e ect. RIE-1 cells were engineered to overexpress human cyclin D1 under the control of a tetracycline-repressible promoter. These cells entered S phase in the presence of TGF-b1 only when human cyclin D1 was derepressed by the withdrawal of tetracycline. These data indicate that TGF-b1 inhibits the synthesis of cyclin D1 in gut epithelial cells and that this inhibition is the cause, rather than the result, of TGF-b1-mediated arrest of intestinal epithelial cell proliferation.

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Cell proliferation studies in the intestinal epithelium of the rat I. Determination of the kinetic parameters

Cited by 344 publications

References 10 publications

Kinetics of changes in the crypts of the jejunal mucosa of dimethylhydrazine-treated rats

Kinetics of changes in the crypts of the jejunal mucosa of dimethylhydrazine-treated rats

Biochemistry of Intestinal Development

TGF-β1 effects on proliferation of rat intestinal epithelial cells are due to inhibition of cyclin D1 expression

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