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Important Endpoints and Proliferative Markers to Assess Small Intestinal Injury and Adaptation using a Mouse Model of Chemotherapy-Induced Mucositis

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Progastrin stimulates murine colonic epithelial mitosis after DNA damage.

Penelope D Ottewell¹, Alastair J M Watson, Timothy C Wang

¹Department of Medicine, University of Liverpool, England.

Gastroenterology

|May 6, 2003

Summary

Mice overexpressing progastrin show increased colonic cell division after DNA damage, unlike wild-type or gastrin-overexpressing mice. This suggests progastrin dysregulation contributes to colon cancer risk by impairing cell cycle control following DNA damage.

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Area of Science:

Gastroenterology
Molecular Biology
Oncology

Background:

Transgenic mice overexpressing progastrin exhibit heightened susceptibility to colonic adenomas induced by chemical carcinogens.
This study investigates the role of apoptosis and mitosis regulation in progastrin's effect on murine colonic epithelium following DNA damage.

Purpose of the Study:

To determine if altered apoptosis or mitosis regulation after DNA damage contributes to increased colonic adenoma susceptibility in progastrin-overexpressing mice.
To compare the effects of progastrin overexpression versus amidated gastrin overexpression on colonic cell cycle regulation post-irradiation.

Main Methods:

Assessed apoptosis and mitosis on a cell positional basis in murine intestinal epithelium after gamma-irradiation.
Analyzed progastrin-overexpressing, gastrin-overexpressing, gastrin-knockout, and wild-type mice.
Examined cell cycle regulator expression using gene array and Western blotting.

Main Results:

Gamma-irradiation induced similar apoptosis levels in the small intestine and colon across all mouse models.
Colonic mitosis was significantly inhibited in wild-type, gastrin-knockout, and gastrin-overexpressing mice post-irradiation.
Progastrin-overexpressing mice exhibited persistent colonic mitosis up to 24 hours after gamma-irradiation, with elevated cdk4 and cyclin D1 protein levels.

Conclusions:

Elevated progastrin levels in mice lead to significantly higher colonic mitosis following DNA damage compared to controls.
Sustained expression of cdk4 and cyclin D1 in progastrin-overexpressing mice enables continued cell cycle progression despite DNA damage.
These findings highlight a mechanism by which progastrin may promote colon tumorigenesis through impaired DNA damage response.