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Impaired Junctions and Invaded Macrophages in Oral Epithelia With Oral Pain.

発表形態:
原著論文
主要業績:
主要業績
単著・共著:
共著
発表年月:
2019年04月
DOI:
10.1369/0022155418812405
会議属性:
指定なし
査読:
有り
リンク情報:

日本語フィールド

著者:
Yoshimoto RU, Aijima R, Ohyama Y, Yoshizumi J, Kitsuki T, Ohsaki Y, Cao AL, Danjo A, Yamashita Y, Kiyoshima T, Kido MA
題名:
Impaired Junctions and Invaded Macrophages in Oral Epithelia With Oral Pain.
発表情報:
J Histochem Cytochem.
キーワード:
概要:
Recurrent or chronic oral pain is a great burden for patients. Recently, the links between epithelial barrier loss and disease were extended to include initiation and propagation. To explore the effects of pathohistological changes in oral epithelia on pain, we utilized labial mucosa samples in diagnostic labial gland biopsies from patients with suspected Sjögren's syndrome (SS), because they frequently experience pain and discomfort. In most labial mucosa samples from patients diagnosed with SS, disseminated epithelial cellular edema was prevalent as ballooning degeneration. The disrupted epithelia contained larger numbers of infiltrating macrophages in patients with oral pain than in patients without pain. Immunohistochemistry revealed that edematous areas were distinct from normal areas, with disarranged cell-cell adhesion molecules (filamentous actin, E-cadherin, β-catenin). Furthermore, edematous areas were devoid of immunostaining for transient receptor potential channel vanilloid 4 (TRPV4), a key molecule in adherens junctions. In an investigation on whether impaired TRPV4 affect cell-cell adhesion, calcium stimulation induced intimate cell-cell contacts among oral epithelial cells from wild-type mice, while intercellular spaces were apparent in cells from TRPV4-knockout mice. The present findings highlight the relationship between macrophages and epithelia in oral pain processi
抄録:

英語フィールド

Author:
Yoshimoto RU, Aijima R, Ohyama Y, Yoshizumi J, Kitsuki T, Ohsaki Y, Cao AL, Danjo A, Yamashita Y, Kiyoshima T, Kido MA
Title:
Impaired Junctions and Invaded Macrophages in Oral Epithelia With Oral Pain.
Announcement information:
J Histochem Cytochem.
An abstract:
Recurrent or chronic oral pain is a great burden for patients. Recently, the links between epithelial barrier loss and disease were extended to include initiation and propagation. To explore the effects of pathohistological changes in oral epithelia on pain, we utilized labial mucosa samples in diagnostic labial gland biopsies from patients with suspected Sjögren's syndrome (SS), because they frequently experience pain and discomfort. In most labial mucosa samples from patients diagnosed with SS, disseminated epithelial cellular edema was prevalent as ballooning degeneration. The disrupted epithelia contained larger numbers of infiltrating macrophages in patients with oral pain than in patients without pain. Immunohistochemistry revealed that edematous areas were distinct from normal areas, with disarranged cell-cell adhesion molecules (filamentous actin, E-cadherin, β-catenin). Furthermore, edematous areas were devoid of immunostaining for transient receptor potential channel vanilloid 4 (TRPV4), a key molecule in adherens junctions. In an investigation on whether impaired TRPV4 affect cell-cell adhesion, calcium stimulation induced intimate cell-cell contacts among oral epithelial cells from wild-type mice, while intercellular spaces were apparent in cells from TRPV4-knockout mice. The present findings highlight the relationship between macrophages and epithelia in oral pain processi


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