{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T07:26:10Z","timestamp":1790753170610,"version":"4.1.0"},"reference-count":33,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2023,12,6]],"date-time":"2023-12-06T00:00:00Z","timestamp":1701820800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Cooperative Open Foundation of Research Institute of Petroleum Exploration and Development, PetroChina","award":["2022-JS-2071"],"award-info":[{"award-number":["2022-JS-2071"]}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31972908, 81991500, 81991502, and 82170977"],"award-info":[{"award-number":["31972908, 81991500, 81991502, and 82170977"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005089","name":"beijing municipal natural science foundation","doi-asserted-by":"publisher","award":["7202082"],"award-info":[{"award-number":["7202082"]}],"id":[{"id":"10.13039\/501100005089","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Dent Res"],"published-print":{"date-parts":[[2024,2]]},"abstract":"<jats:p>\n                    Tight junction proteins play a crucial role in paracellular transport in salivary gland epithelia. It is clear that severe xerostomia in patients with HELIX syndrome is caused by mutations in the claudin-10 gene. However, little is known about the expression pattern and role of claudin-10 in saliva secretion in physical and disease conditions. In the present study, we found that only claudin-10b transcript was expressed in human and mouse submandibular gland (SMG) tissues, and claudin-10 protein was dominantly distributed at the apicolateral membranes of acini in human, rat, and mouse SMGs. Overexpression of claudin-10 significantly reduced transepithelial electrical resistance and increased paracellular transport of dextran and Na\n                    <jats:sup>+<\/jats:sup>\n                    in SMG-C6 cells. In C57BL\/6 mice, pilocarpine stimulation promoted secretion and cation concentration in saliva in a dose-dependent increase. Assembly of claudin-10 to the most apicolateral portions in acini of SMGs was observed in the lower pilocarpine (1 mg\/kg)\u2013treated group, and this phenomenon was much obvious in the higher pilocarpine (10 mg\/kg)\u2013treated group. Furthermore, 7-, 14-, and 21-wk-old nonobese diabetic (NOD) and BALB\/c mice were used to mimic the progression of hyposalivation in Sj\u00f6gren syndrome. Intensity of claudin-10 protein was obviously lower in SMGs of 14- and 21-wk-old NOD mice compared with that of age-matched BALB\/c mice. In the cultured mouse SMG tissues, interferon-\u03b3 (IFN-\u03b3) downregulated claudin-10 expression. In claudin-10\u2013overexpressed SMG-C6 cells, paracellular permeability was decreased. Furthermore, IFN-\u03b3 stimulation increased p-STAT1 level, whereas pretreatment with JAK\/STAT1 antagonist significantly alleviated the IFN-\u03b3\u2013induced claudin-10 downregulation. These results indicate that claudin-10 functions as a pore-forming component in acinar epithelia of SMGs, assembly of claudin-10 is required for saliva secretion, and downregulation of claudin-10 induces hyposecretion. These findings may provide new clues to novel therapeutic targets on hyposalivation.\n                  <\/jats:p>","DOI":"10.1177\/00220345231210547","type":"journal-article","created":{"date-parts":[[2023,12,7]],"date-time":"2023-12-07T02:00:26Z","timestamp":1701914426000},"page":"167-176","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":8,"title":["Claudin-10 Decrease in the Submandibular Gland Contributes to Xerostomia"],"prefix":"10.1177","volume":"103","author":[{"given":"L.","family":"He","sequence":"first","affiliation":[{"name":"Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Beijing, P. R. 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