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)

Hyposecretion of saliva and consequent dry mouth lead to severe caries and periodontal disease. Therapeutic radiation for head and neck cancer and sialadenitis result in atrophy and fibrosis of salivary glands, but the mechanism is not clear. As a model for dysfunction of salivary glands, we examined the change of gene expression patterns in primary cultured parotid acinar cells. The expression levels of acinar markers such as amylase and aquaporin-5 rapidly decreased during culture. At the same time, ductal markers began to be expressed although their expression was transient. In the late phase of culture, markers of epithelial-mesenchymal transition began to be expressed and increased. Inhibitor for Src or p38 MAP kinase suppressed these changes. These results suggest that parotid acinar cells transiently change to duct-like cells during epithelial-mesenchymal transition and that these changes are induced by signal transduction via Src-p38 MAP kinase pathway. There is a possibility that parotid acinar cells retain a plasticity of differentiation.
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PMID:Parotid acinar cells transiently change to duct-like cells during epithelial-mesenchymal transition. 2022 94

Although xerostomia can cause persistent oral pain, the mechanisms underlying such pain are not well understood. To evaluate whether a phosphorylated p38 (pp38)-TRPV4 mechanism in trigeminal ganglion (TG) neurons has a role in mechanical hyperalgesia of dry tongue, a rat model of dry tongue was used to study the nocifensive reflex and pp38 and TRPV4 expression in TG neurons. The head-withdrawal reflex threshold for mechanical stimulation of the tongue was significantly lower in dry-tongue rats than in sham rats. The numbers of TRPV4- and pp38-immunoreactive cells in the TG were significantly higher in dry-tongue rats than in sham rats. Many TRPV4-IR cells were also pp38-immunoreactive. The number of TRPV1-IR cells was unchanged in the TG after induction of tongue dryness. Local injection of a TRPV4 blocker attenuated tongue mechanical hypersensitivity in dry-tongue rats. Intraganglionic injection of a selective p38 MAP kinase inhibitor eliminated tongue hypersensitivity in dry-tongue rats and suppressed TRPV4 expression in TG neurons. The present findings suggest that TRPV4 activation via p38 phosphorylation in TG neurons is involved in mechanical hypersensitivity associated with dry tongue. These mechanisms may have a role in pain associated with xerostomia.
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PMID:Involvement of TRPV4 ionotropic channel in tongue mechanical hypersensitivity in dry-tongue rats. 3199 16