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Although substantial evidence has demonstrated that incubation under an inflammatory condition may accelerate senescence of PDLSCs, whether cellular senescence in response to inflammatory incubation contributes to cell dysfunction remain unexplored. In this study, we first observed inflammation\u2010caused PDLSC senescence in periodontitis based on comparisons of matched patients, and this cellular senescence was demonstrated in healthy cells that were subjected to inflammatory conditions. We subsequently designed further experiments to investigate the possible mechanism underlying inflammation\u2010induced PDLSC senescence with a particular focus on the role of long noncoding RNAs (lncRNAs). LncRNA microarray analysis and functional gain\/loss studies revealed <jats:italic>SLC30A4\u2010AS1<\/jats:italic> as a regulator of inflammation\u2010mediated PDLSC senescence. By full\u2010length transcriptome sequencing, we found that <jats:italic>SLC30A4\u2010AS1<\/jats:italic> interacted with SRSF3 to affect the alternative splicing (AS) of <jats:italic>TP53BP1<\/jats:italic> and alter the expression of <jats:italic>TP53BP1<\/jats:italic>\u2010204. Further functional studies showed that decreased expression of <jats:italic>TP53BP1<\/jats:italic>\u2010204 reversed PDLSC senescence, and <jats:italic>SLC30A4\u2010AS1<\/jats:italic> overexpression\u2010induced PDLSC senescence was abolished by <jats:italic>TP53BP1<\/jats:italic>\u2010204 knockdown. Our data suggest for the first time that <jats:italic>SLC30A4\u2010AS1<\/jats:italic> plays a key role in regulating PDLSC senescence in inflammatory environments by modulating the AS of <jats:italic>TP53BP1<\/jats:italic>.<\/jats:p>","DOI":"10.1111\/cpr.13778","type":"journal-article","created":{"date-parts":[[2024,11,22]],"date-time":"2024-11-22T02:24:48Z","timestamp":1732242288000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["<scp><i>SLC30A4\u2010AS1<\/i><\/scp> Mediates the Senescence of Periodontal Ligament Stem Cells in Inflammatory Environments via\u00a0the Alternative Splicing of <scp><i>TP53BP1<\/i><\/scp>"],"prefix":"10.1111","volume":"58","author":[{"given":"Mei","family":"Xu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Oral &amp; Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for 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