{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T17:54:49Z","timestamp":1791482089655,"version":"4.3.4"},"reference-count":26,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,8,25]],"date-time":"2022-08-25T00:00:00Z","timestamp":1661385600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DE021052 (SN)"],"award-info":[{"award-number":["DE021052 (SN)"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DE026259 (ARN)"],"award-info":[{"award-number":["DE026259 (ARN)"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DE027980 (ARN)"],"award-info":[{"award-number":["DE027980 (ARN)"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008522","name":"University of Illinois at Chicago","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008522","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Clinic Periodontology"],"published-print":{"date-parts":[[2023,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>To evaluate the potential role of miR\u201026 family members in periodontal pathogenesis by assessing innate immune responses to periopathic bacteria and regulation of cytoskeletal organization.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      Expression of miR\u201026a\u20105p and miR\u201026b\u20105p was quantified in gingival biopsies derived from healthy and periodontally diseased subjects before and after non\u2010surgical (scaling and root planing) therapy by RT\u2010qPCR. Global pathway analysis and luciferase assays were performed for target identification and validation. Cytokine expression was assessed in miR\u201026a\u20105p transfected human oral keratinocytes upon stimulation with either live\n                      <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                      (\n                      <jats:italic>Pg<\/jats:italic>\n                      ),\n                      <jats:italic>Aggregatibacter actinomycetemcomitans<\/jats:italic>\n                      or\n                      <jats:italic>Pg<\/jats:italic>\n                      lipopolysaccharide (LPS). Wound closure assays were performed in cells transfected with miR\u201026a\u20105p, while the impact on cytoskeletal organization was assessed by F\u2010actin staining.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>miR\u201026a\u20105p and miR\u201026b\u20105p were downregulated in diseased gingiva and restored 4\u20136\u2009weeks post\u2010therapy to levels comparable with healthy subjects. Target validation assays identified phospholipase C beta 1 as a bona fide novel target exhibiting antagonistic expression pattern in disease and post\u2010therapy cohorts. miR\u201026a\u20105p transfected cells secreted higher levels of cytokine\/chemokines upon stimulation with periopathogens and demonstrated impaired cell migration and cytoskeletal rearrangement.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Downregulated miR\u201026a\u20105p levels in periodontal inflammation may interfere with key cellular functions that may have significant implications for host defence and wound healing.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jcpe.13715","type":"journal-article","created":{"date-parts":[[2022,8,4]],"date-time":"2022-08-04T07:05:48Z","timestamp":1659596748000},"page":"102-113","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Downregulation of\n                    <scp>miRNA<\/scp>\n                    \u201026 in chronic periodontitis interferes with innate immune responses and cell migration by targeting phospholipase\n                    <scp>C<\/scp>\n                    beta 1"],"prefix":"10.1111","volume":"50","author":[{"given":"Juhi R.","family":"Uttamani","sequence":"first","affiliation":[{"name":"Department of Periodontics, College of Dentistry and Dental Clinics University of Iowa  Iowa City Iowa USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Afsar R.","family":"Naqvi","sequence":"additional","affiliation":[{"name":"Department of Periodontics, College of Dentistry University 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