E2F1-deficient NOD/SCID mice are an experimental model for dry mouth

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  • Satoh Keitaro
    Department of Regulatory Physiology, Dokkyo Medical University School of Medicine Department of Physiology, Nihon University School of Dentistry at Matsudo
  • Narita Takanori
    Department of Physiology, Nihon University School of Dentistry at Matsudo
  • Matsui-Inohara Hikaru
    Department of Bacteriology, National Institute of Infectious Diseases
  • Ito Tatsuro
    Department of Bacteriology, National Institute of Infectious Diseases
  • Senpuku Hidenobu
    Department of Bacteriology, National Institute of Infectious Diseases
  • Sugiya Hiroshi
    Department of Physiology, Nihon University School of Dentistry at Matsudo

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Abstract

Saliva contains a wide variety of secretory proteins, including α-amylase, lysozyme, peroxidase, immunoglobulins, and mucins. Hyposecretion of saliva and consequent dry mouth will lead to severe dental caries, periodontal disease, and mucosal infections, resulting in degrade of quality of life. Polyposia development is one of sign usually seen in dry mouth patients. However, little is reported in dry mouth-model animal regarding the entire process of polyposia development. We investigated the behavior of polyposia in E2F1-deficient non-obese diabetic/severe combined immunodeficiency disease (NOD/SCID) mice, as a dry mouth-model. E2F1-deficient NOD/SCID mice secreted small amount of saliva under the stimulation with a cholinergic agonist, pilocarpine, compared with control mice. The frequency of water intake by E2F-1-deficient NOD/SCID mice was more than that by control mice. These results suggest that E2F-1-deficient NOD/SCID mice show a behavior similar to polyposia and are very useful experimental model of dry mouth patients. J. Med. Invest. 56 Suppl.: 260-261, December, 2009

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