{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,2]],"date-time":"2026-03-02T10:50:11Z","timestamp":1772448611643,"version":"3.50.1"},"reference-count":39,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2022,6,2]],"date-time":"2022-06-02T00:00:00Z","timestamp":1654128000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To explore the role of Marginal Zone B and B\u20101 Cell\u2010Specific Protein (MZB1), a novel molecule associated with periodontitis, in migration of human periodontal ligament cells (hPDLCs) and alveolar bone orchestration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Background<\/jats:title><jats:p>MZB1 is an ER\u2010localized protein and its upregulation has been found to be associated with a variety of human diseases. However, few studies have investigated the effect and mechanism of MZB1 on hPDLCs in periodontitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Gene expression profiles in human gingival tissues were acquired from the Gene Expression Omnibus (GEO) database, and candidate molecules were then selected through bioinformatic analysis. Subsequently, we identified the localization and expression of MZB1 in human gingival tissues, mice, and hPDLCs by immunofluorescence, RT\u2010qPCR, and Western blot. Dual\u2010luciferase reporter assay was applied to assess the binding of miR\u2010185\u20105p to MZB1. Furthermore, the effects of MZB1 on cell migration, proliferation, and apoptosis in vitro were investigated by wound\u2010healing assay, transwell assay, CCK\u20108 assay, and flow cytometry analysis. Finally, Micro\u2010CT analysis and H&amp;E staining were performed to examine the effects of MZB1 on alveolar bone loss in vivo.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Bioinformatic analysis discovered that MZB1 was one of the most significantly increased genes in periodontitis patients. MZB1 was markedly increased in the gingival tissues of periodontitis patients, in the mouse models, and in the hPDLCs treated with lipopolysaccharide of <jats:italic>Porphyromonas gingivalis<\/jats:italic> (LPS\u2010PG). Furthermore, in vitro experiments showed that MZB1, as a target gene of miR\u2010185\u20105p, inhibited migration of hPDLCs. Overexpression of MZB1 specifically upregulated the phosphorylation of p65, while pretreatment of MZB1\u2010overexpressed hPDLCs with PDTC (NF\u2010\u03baB inhibitor) notably reduced the p\u2010p65 level and promoted cell migration. In addition, the mRNA expression levels of alkaline phosphatase (ALP) and Runt\u2010related transcription factor 2 (Runx2) were inhibited in MZB1\u2010overexpressed hPDLCs and miR\u2010185\u20105p inhibitor treated hPDLCs, respectively. In vivo experiments showed that knockdown of MZB1 alleviated the loss of alveolar bone.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>As a target gene of miR\u2010185\u20105p, MZB1 plays a crucial role in inhibiting the migration of hPDLCs through NF\u2010\u03baB signaling pathway and deteriorating alveolar bone loss.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.13014","type":"journal-article","created":{"date-parts":[[2022,6,2]],"date-time":"2022-06-02T18:01:17Z","timestamp":1654192877000},"page":"811-823","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["<scp>MZB1<\/scp> targeted by <scp>miR<\/scp>\u2010185\u20105p inhibits the migration of human periodontal ligament cells through <scp>NF\u2010\u03baB<\/scp> signaling and promotes alveolar bone loss"],"prefix":"10.1111","volume":"57","author":[{"given":"Dingyi","family":"Li","sequence":"first","affiliation":[{"name":"Department of 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