Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043352 (xerostomia)
 4,250 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Saliva contains a wide variety of secretory proteins, including alpha-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.
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PMID:E2F1-deficient NOD/SCID mice are an experimental model for dry mouth. 2022 95

Non-obese diabetic (NOD) mice have been used as a model for dry mouth. NOD mice lacking the gene encoding E2f1, a transcription factor, develop hyposalivation more rapidly progressively than control NOD mice. However, the model mice are associated with an underlying disease such as diabetes. We have now established E2f1-deficient NOD/severe combined immunodeficiency disease (NOD/SCID.E2f1(-/-)) mice to avoid the development of diabetes (Matsui-Inohara et al., Exp Biol Med (Maywood) 234(12):1525-1536, 2009). In this study, we investigated the pathophysiological features of dry mouth using NOD/SCID.E2f1(-/-) mice. In NOD/SCID.E2f1(-/-) mice, the volume of secreted saliva stimulated with pilocarpine is about one third that of control NOD/SCID mice. In behavioral analysis, NOD/SCID.E2f1(-/-) mice drank plenty of water when they ate dry food, and the frequency and time of water intake were almost double compared with control NOD/SCID mice. Histological analysis of submandibular glands with hematoxylin-eosin stain revealed that NOD/SCID.E2f1(-/-) mice have more ducts than NOD/SCID mice. In western blot analysis, the expression of aquaporin 5 (AQP5), a marker of acinar cells, in parotid and in submandibular glands of NOD/SCID.E2f1(-/-) mice was lower than in NOD/SCID mice. Immunohistochemical analysis of parotid and submandibular acini revealed that the localization of AQP5 in NOD/SCID.E2f1(-/-) mice differs from that in NOD/SCID mice; AQP5 was leaky and diffusively localized from the apical membrane to the cytosol in NOD/SCID.E2f1(-/-) mice. The ubiquitination of AQP5 was detected in submandibular glands of NOD/SCID.E2f1(-/-) mice. These findings suggest that the change of acinar/duct structure and the down-regulation of AQP5 in the salivary gland cause the pathogenesis of hyposalivation in NOD/SCID.E2f1(-/-) mice.
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PMID:E2f1-deficient NOD/SCID mice have dry mouth due to a change of acinar/duct structure and the down-regulation of AQP5 in the salivary gland. 2317 81