Recruitment of Cells in the Small Intestine into Rapid Cell Cycle by Small Doses of External γ or Internal β-radiation

Tsubouchi, Susumu; Potten, Christopher S

doi:10.1080/09553008514551361

Cited by 23 publications

(17 citation statements)

References 13 publications

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“…The rationale for this design is to distinguish between the regenerative cell divisions under normal circumstances and the compensatory cell divisions for apoptotic losses. The instantaneous time scale for replenishing cell divisions is extrapolated from the observation that under strong external stimuli, the rate of progression through the cell cycle is accelerated; for instance, ionizing radiation was shown to induce proliferative activity [42] and shorten the duration of the cell cycle [43]. In addition, thermal injury [44] and starvation-induced stress [45] also tend to increase mitotic activity.…”

Section: Methodsmentioning

confidence: 99%

Patterns of Proliferative Activity in the Colonic Crypt Determine Crypt Stability and Rates of Somatic Evolution

Zhao

Michor

2013

PLoS Comput Biol

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Epithelial cells in the colon are arranged in cylindrical structures called crypts in which cellular proliferation and migration are tightly regulated. We hypothesized that the proliferation patterns of cells may determine the stability of crypts as well as the rates of somatic evolution towards colorectal tumorigenesis. Here, we propose a linear process model of colonic epithelial cells that explicitly takes into account the proliferation kinetics of cells as a function of cell position within the crypt. Our results indicate that proliferation kinetics has significant influence on the speed of cell movement, kinetics of mutation propagation, and sensitivity of the system to selective effects of mutated cells. We found that, of all proliferation curves tested, those with mitotic activities concentrated near the stem cell, including the actual proliferation kinetics determined in in vivo labeling experiments, have a greater ability of delaying the rate of mutation accumulation in colonic stem cells compared to hypothetical proliferation curves with mitotic activities focused near the top of the crypt column. Our model can be used to investigate the dynamics of proliferation and mutation accumulation in spatially arranged tissues.

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Section: Methodsmentioning

confidence: 99%

Patterns of Proliferative Activity in the Colonic Crypt Determine Crypt Stability and Rates of Somatic Evolution

Zhao

Michor

2013

PLoS Comput Biol

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“…Transit generations 5-9 >5-9 + absolute count; * assuming a 0.6 geometric correction factor; # depends on position, 300 for caecum, 450 for rectum; a Kellett [45]; b Wright and Alison [5]; c Potten [13]. architectural and structural organisation at the cellular level is illustrated in Figs I and 2 and the size of the proliferative compartments and the cell kinetics are summarised in Figs 3 and 4.…”

Section: Figmentioning

confidence: 99%

“…Three independent and totally different types of experiment have all illustrated that the killing of a very small number of cells in the stem cell region elicits rapid (immediate) changes in the proliferation in the remaining cells [7,8]. The cell cycle in this region of the crypt is shortened dramatically [43,45,46]. Using a functional assay for stem cells it can be shown that they are recruited into rapid proliferation.…”

Section: Figmentioning

confidence: 99%

The significance of spontaneous and induced apoptosis in the gastrointestinal tract of mice

1992

Self Cite

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The crypts of the gastrointestinal mucosa are highly structured and polarised organs with rapid cell proliferation and an hierarchical organisation with relatively few stem cells. These tend to be located at specific positions in the tissue--at the crypt base in the colon and about four cell positions from the base (above the Paneth cells) in the small intestine. A small but constant level of spontaneous cell death occurs in the crypt. The levels of cell death are elevated by small exposures to radiation or cytotoxic drugs. The morphology of the cell death is typical of apoptosis. The maximum yield of cell death following cytotoxic exposure is observed at about 3-6 h after treatment and for many agents the death is characteristically located at the fourth (stem) cell position in the small intestine. The significance and implications of these observations are discussed in relation to the internal screening and programming within damage cells and with respect to tissue homeostatic mechanisms.

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“…Because Pls1 Ϫ/Ϫ mice do not display an overt phenotype, the increased fragility of the BB and the increased rate of cell death could be balanced by the elevated rate of cell migration. A possible explanation for the lack of evidence of an increased number of proliferating cells in the crypts of the Pls1 Ϫ/Ϫ mice is a shortening of the cell cycle of the stem cell population as reported for example after gamma or beta irradiation of the intestine (Tsubouchi and Potten, 1985).…”

Section: Pls1mentioning

confidence: 99%

Plastin 1 Binds to Keratin and Is Required for Terminal Web Assembly in the Intestinal Epithelium

Grimm-Günter

Revenu

Ramos

et al. 2009

MBoC

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Plastin 1 (I-plastin, fimbrin) along with villin and espin is a prominent actin-bundling protein of the intestinal brush border microvilli. We demonstrate here that plastin 1 accumulates in the terminal web and interacts with keratin 19, possibly contributing to anchoring the rootlets to the keratin network. This prompted us to investigate the importance of plastin 1 in brush border assembly. Although in vivo neither villin nor espin is required for brush border structure, plastin 1-deficient mice have conspicuous ultrastructural alterations: microvilli are shorter and constricted at their base, and, strikingly, their core actin bundles lack true rootlets. The composition of the microvilli themselves is apparently normal, whereas that of the terminal web is profoundly altered. Although the plastin 1 knockout mice do not show any overt gross phenotype and present a normal intestinal microanatomy, the alterations result in increased fragility of the epithelium. This is seen as an increased sensitivity of the brush border to biochemical manipulations, decreased transepithelial resistance, and increased sensitivity to dextran sodium sulfate-induced colitis. Plastin 1 thus emerges as an important regulator of brush border morphology and stability through a novel role in the organization of the terminal web, possibly by connecting actin filaments to the underlying intermediate filament network.

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Recruitment of Cells in the Small Intestine into Rapid Cell Cycle by Small Doses of External γ or Internal β-radiation

Cited by 23 publications

References 13 publications

Patterns of Proliferative Activity in the Colonic Crypt Determine Crypt Stability and Rates of Somatic Evolution

Patterns of Proliferative Activity in the Colonic Crypt Determine Crypt Stability and Rates of Somatic Evolution

The significance of spontaneous and induced apoptosis in the gastrointestinal tract of mice

Plastin 1 Binds to Keratin and Is Required for Terminal Web Assembly in the Intestinal Epithelium

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