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No difference in the level of gastric mucosal cell apoptosis and proliferation in Helicobacter pylori-colonized p53 heterozygous knockout mice

  1. H. Suzuki1,
  2. M. Miyazawa1,
  3. A. Kai2,
  4. M. Suzuki3,
  5. M. Suematsu4,
  6. S. Miura5,
  7. H. Ishii1

Article first published online: 20 APR 2002

DOI: 10.1046/j.1365-2036.16.s2.18.x

Issue

Alimentary Pharmacology & Therapeutics

Alimentary Pharmacology & Therapeutics

Volume 16, Issue Supplement s2, pages 158–166, April 2002

Additional Information

How to Cite

Suzuki, H. , Miyazawa, M. , Kai, A. , Suzuki, M. , Suematsu, M. , Miura, S. and Ishii, H. (2002), No difference in the level of gastric mucosal cell apoptosis and proliferation in Helicobacter pylori-colonized p53 heterozygous knockout mice. Alimentary Pharmacology & Therapeutics, 16: 158–166. doi: 10.1046/j.1365-2036.16.s2.18.x

Author Information

  1. 1

    Department of Internal Medicine, & Biochemistry and Integrative Medical Biology, School of Medicine, Keio University, Japan,

  2. 2

    Tokyo Metropolitan Research Laboratory of Public Health, Tokyo, Japan,

  3. 3

    Department of Gastroenterology, National Tokyo Medical Center, Tokyo, Japan,

  4. 4

    Biochemistry and Integrative Medical Biology, School of Medicine, Keio University, Japan,

  5. 5

    Second Department of Internal Medicine, National Defense Medical College, Saitama, Japan

* Dr H. Suzuki, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail: hsuzuki@sc.itc.keio.ac.jp

Publication History

  1. Issue published online: 20 APR 2002
  2. Article first published online: 20 APR 2002

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Background:

We previously reported that attenuated epithelial apoptosis and enhanced proliferation in comparison with mice might link to the specific carcinogenesis in Mongolian gerbils and suggested that the difference in both strains might be due to a difference in genetic background. p53 is a well-known tumour suppressor gene, mutation of which is also known to be involved in gastric cancer formation.

Aim:

The present study was designed to examine the level of gastric epithelial apoptosis and proliferation in p53 heterozygous knockout mice (p53+/−) colonized with Helicobacter pylori(Sydney strain: SS1).

Methods:

Female p53+/− mice and wild-type controls were orally inoculated with SS1 and the stomachs were examined 24 weeks later. DNA fragmentation was measured by levels of cytoplasmic mono- & oligo-nucleosomes as well as by the TUNEL method. Gastric mucosal proliferative activity was morphometrically evaluated from the PCNA-stained tissue specimens. Gastric mucosal myeloperoxidase (MPO) activity was measured to evaluate mucosal inflammation.

Results:

DNA fragmentation and the number of TUNEL-positive cells, as well as PCNA-positive cell number increased significantly in both groups of H. pylori-infected mice, suggesting that levels of apoptosis and proliferation may be independent of a deficiency of one p53 allele. MPO activity in p53+/− mice and wild-type controls increased to the same level.

Conclusion:

Although H. pylori inoculation per se induces an increase in cell turnover in mice, heterozygous mutation of p53 did not significantly modify the balance in cell apoptosis and proliferation.

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