{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T16:40:12Z","timestamp":1787244012862,"version":"build-2736575974"},"reference-count":70,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,8,9]],"date-time":"2012-08-09T00:00:00Z","timestamp":1344470400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    It is well known that the aryl hydrocarbon receptor (AhR) is involved in the toxicity of halogenated aromatic hydrocarbons (HAH) and polycyclic aromatic hydrocarbons (PAH). Recent experiments have shown the induction of impaired tooth and hard\u2010tissue formation by AhR pathway activation, however, the effect on periodontal ligament (PDL) tissue remains unclear. Here, we investigated the effects of benzo(a)pyrene (BaP), a member of PAH, on the extracellular matrix (ECM) remodeling\u2010related molecules, collagen type I (COL\u2010I), matrix metalloproteinase\u20101 (MMP\u20101), alpha\u2010smooth muscle actin (\u03b1\u2010SMA) expression, and apoptosis in two different human periodontal ligament cells (HPDLCs). The transduction of AhR from the cytoplasm to the nucleus and the increase of AhR\u2010responsive genes; that is,\n                    <jats:italic>cytochrome P450 1A1<\/jats:italic>\n                    (\n                    <jats:italic>CYP1A1<\/jats:italic>\n                    ),\n                    <jats:italic>cytochrome P450 1B1<\/jats:italic>\n                    (\n                    <jats:italic>CYP1B1<\/jats:italic>\n                    ), and\n                    <jats:italic>aryl\u2010hydrocarbon receptor repressor<\/jats:italic>\n                    (\n                    <jats:italic>AhRR<\/jats:italic>\n                    ), expression was induced by BaP exposure in both HPDLCs. BaP treatment significantly enhanced\n                    <jats:italic>MMP\u20101<\/jats:italic>\n                    mRNA expression and MMP\u20101 protein production, while markedly suppressing\n                    <jats:italic>COL\u2010I<\/jats:italic>\n                    and\n                    <jats:italic>a\u2010SMA<\/jats:italic>\n                    mRNA expression in both HPDLCs. Furthermore, these BaP\u2010treated HPDLCs fell into apoptotic cell death as evidenced by induction in annexin V and caspase\u20103\/7 staining and reduction of total cell number and\n                    <jats:italic>Bcl\u20102<\/jats:italic>\n                    mRNA expression. Thus, BaP exposure altered the expression of ECM\u2010related molecules and induced apoptosis in HPDLCs through activation of the AhR pathway. Overactivity of the AhR pathway may induce an inappropriate turnover of PDL tissue via disordered ECM remodeling and apoptosis in PDL cells. J. Cell. Biochem. 113: 3093\u20133103, 2012. \u00a9 2012 Wiley Periodicals, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jcb.24186","type":"journal-article","created":{"date-parts":[[2012,5,11]],"date-time":"2012-05-11T11:57:02Z","timestamp":1336737422000},"page":"3093-3103","source":"Crossref","is-referenced-by-count":23,"title":["Alternation of extracellular matrix remodeling and apoptosis by activation of the aryl hydrocarbon receptor pathway in human periodontal ligament cells"],"prefix":"10.1002","volume":"113","author":[{"given":"Atsushi","family":"Tomokiyo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hidefumi","family":"Maeda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinsuke","family":"Fujii","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoshi","family":"Monnouchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naohisa","family":"Wada","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiyomi","family":"Hori","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katsuaki","family":"Koori","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naohide","family":"Yamamoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoko","family":"Teramatsu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akifumi","family":"Akamine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,8,9]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(90)90337-T"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s10439-006-9090-z"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1875-595X.2006.tb00336.x"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1902\/jop.1995.66.7.552"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041590120"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1177\/39.1.1983870"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.19.11595"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.106.3.761"},{"key":"e_1_2_6_10_1","doi-asserted-by":"crossref","first-page":"8907","DOI":"10.1016\/S0021-9258(19)40671-6","article-title":"Proteins of the periodontium. 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