The Cell Cycle Time in the Rat Jejunal Mucosa

The detailed temporal and spatial changes in the labelling index in crypts of the small intestine of the mouse have been analysed after 8.0 Gy gamma-irradiation. The labelling index was determined for each cell position in the crypts at 34 different times between 3 and 192 h after irradiation. The changes between consecutive time points have been analysed to determine the details of the crypt shrinkage and crypt repopulation phenomena. The following points can be made: (1) There is a dramatic reduction in the overall labelling of the crypt which begins within 3 h and is at its minimum by 15 h postirradiation. Most of this shrinkage can be attributed to continued near-normal emigration of cells from the crypt to the villus while mitosis is reduced or absent, and a possibly premature maturation within the transit population. (2) The labelling index never falls below 34 per cent of control, i.e. many labelled cells persist and continue to replicate their DNA at all times postirradiation. (3) Repopulation begins in the lower regions of the crypt. The first changes are an increase in labelling at cell positions 3-8 that begins at 3 h and reaches a peak at 12 h. There is a second increase in proliferation at the crypt base that begins at about 15 h and reaches a peak at 22-32 h postirradiation. There is a third peak which begins at about 46 h and reaches a peak at 60-70 h. (4) There is a reduction in proliferation at the crypt base that begins at about 72 h postirradiation. (5) The mid and upper crypt population shrinks initially to reach a minimum at about 15 h, after which there is a steady increase to reach a peak at about 72 h. The labelling spreads into the crypt-villus boundary area beginning at about 32 h. There is a reduction of proliferative activity in the mid-crypt region that begins at about 72 h. (6) There is a dramatic overshoot in overall labelling index at 72 h, which involves mainly the upper crypt. This does not revert to normal levels within the 192 h time scale of the present experiments. There is a mild overshoot in labelling at the crypt base at 48-78 h with a return to normal levels thereafter.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…1986) . Similar distributions have been presented by other groups (Al-Dewachi et al 1974, 1979, Wright and Alison 1984, Cairnie et al . 1965 .…”

Section: 6 Data Presentationsupporting

confidence: 90%

The Temporal and Spatial Changes in Cell Proliferation within the Irradiated Crypts of the Murine Small Intestine

Potten

Owen

Roberts

1990

International Journal of Radiation Biology

116

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“…30,31 PCNA is synthesized in late G 1 and Sphase. 30,31 The half-life of PCNA is approximately 12 h. 30,31 It is also known that the length of the G 1 -phase in cells in the jejunal crypts of rats in normal conditions is 3-6 h, the length of the S-phase is 6-8 h, the G 2 -phase proceeds for 0.5-2 h, and mitosis requires about 1 h. 32,33 In jejunal crypt epithelial cells, PCNA can therefore be present in the G 1 , S, G 2 , and M-phases, but not in the G 0 -phase. In the esophageal epithelium, the length of the G 1 -phase is about 17-20 h, the S-phase proceeds for approximately 7-8 h, the G 2 -phase continues for 1-2 h, and mitosis requires about 1 h. 34,35 Hence, PCNA can be found mainly in esophageal epithelial cells which are in late G 1 and S-phases of the cell cycle.…”

Section: Discussionmentioning

confidence: 99%

Effect of acute and chronic glucocorticoid treatments on epithelial cell proliferation in the esophagus and small intestine of rats

Гунин

Nikolaev

1999

Journal of Gastroenterology

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Data about glucocorticoid influence on proliferation in the esophagus and small intestine are very contradictory and need to be reexamined. Moreover, only the effects of acute or short-term treatments with glucocorticoids have been demonstrated, whereas nothing is known about their effects under chronic exposure. This work was therefore carried out to examine proliferative activity in the esophagus and small intestine under conditions of acute and chronic glucocorticoid exposure. Rats were treated with either glucocorticoid triamcinolone acetonide or vehicle for 3, 33, or 63 days. Proliferation was assessed in the basal layer of esophageal epithelium and in the epithelium of jejunal crypts, using three criteria, as the number of mitotic, bromodeoxyuridine-labelled, and proliferating cell nuclear antigen-labelled cells. Treatment with glucocorticoid for 3 days led to a slight decrease in all parameters in the esophageal epithelium and had almost no effect on proliferation in the epithelium of jejunal crypts. Long-term treatment with glucocorticoid for either 33 or 63 days resulted in an increase in all parameters tested in both esophageal and jejunal crypt epithelia. Sixty-three-day treatment had a more prominent and significant (P < 0.05) effect. These results suggest that acute glucocorticoid treatment nonsignificantly reduces the number of cells in the cell cycle in the esophageal epithelium, whereas chronic treatment increases the number of proliferating cells in both esophageal and jejunal crypt epithelia.

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“…These transverse sections were processed through to paraffin wax and serial 3 ,um sections were prepared and stained with haematoxylin and eosin and periodic acid/ Schiff with and without amylase. Microautoradiographs were also prepared in the usual way (Al-Dewachi et al, 1974). All neoplasms were categorized histologically into subgroups (see Results section).…”

Section: Methodsmentioning

confidence: 99%

“…5c represents the pooled whole-crypt data. Table I summarizes the estimates of duration of the cell cycle (Tc) and the DNA-synthetic phase (ts) in DMH-treated animals and in normal animals from the same colony (Al-Dewachi et al, 1974).…”

Section: H-tdr Labellingmentioning

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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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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The Cell Cycle Time in the Rat Jejunal Mucosa

Cited by 17 publications

References 7 publications

The Temporal and Spatial Changes in Cell Proliferation within the Irradiated Crypts of the Murine Small Intestine

The Temporal and Spatial Changes in Cell Proliferation within the Irradiated Crypts of the Murine Small Intestine

Effect of acute and chronic glucocorticoid treatments on epithelial cell proliferation in the esophagus and small intestine of rats

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

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