{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,12,19]],"date-time":"2024-12-19T05:28:35Z","timestamp":1734586115530,"version":"3.30.2"},"reference-count":32,"publisher":"Scientific Scholar","content-domain":{"domain":["cytojournal.com"],"crossmark-restriction":true},"short-container-title":["Cytojournal"],"abstract":"\nObjective:<\/jats:title>\nMany different types of infectious oral diseases have been identified clinically, including chronic periodontitis. Porphyromonas gingivalis<\/jats:italic> is the main pathogen causing chronic periodontitis, which is closely related to atherosclerosis (AS) and can promote the expression levels of caveolin 1 (Cav-1) and induced ribonucleic acid (RNA)-binding protein human antigen R (HuR). However, the roles of Cav-1 and its relationship with HuR in P. gingivalis<\/jats:italic>-mediated AS progression remain largely unknown. Here, we aimed to detect the role and molecular mechanisms of Cav-1 in P. gingivalis<\/jats:italic>-mediated AS.<\/jats:p>\n<\/jats:sec>\n\nMaterial and Methods:<\/jats:title>\nTo investigate the role of Cav-1 in P. gingivalis<\/jats:italic>-mediated AS, we infected human umbilical vein endothelial cells (HUVECs) with P. gingivalis<\/jats:italic> at a multiplicity of infection of 100:1 for 6, 12, and 24 h to simulate P. gingivalis-<\/jats:italic>induced AS models in vitro<\/jats:italic> and then transfected them with Cav-1 small interfering RNA to silence Cav-1. Combining molecular biology experimental techniques such as cell counting kit-8 assay, enzyme-linked immunosorbent assay, immunofluorescence staining, flow cytometry, Western blotting, and Oil Red O staining, and apolipoprotein E-deficient AS model mice, the impacts of Cav-1 on cell viability, inflammation, oxidative stress, apoptosis, Cav-1 and intercellular cell adhesion molecule-1 (ICAM-1) levels, and atherosclerotic plaque formation were investigated. Then, the relationship between Cav-1 and HuR was investigated through biotin pull-down and RNA immunoprecipitation assays, reverse transcription quantitative polymerase chain reaction, and Western blot.<\/jats:p>\n<\/jats:sec>\n\nResults:<\/jats:title>\nP. gingivalis<\/jats:italic> can induce Cav-1 expression in a time- and dose-dependent manner (P<\/jats:italic> < 0.05). This effect can inhibit the proliferation of HUVECs (P<\/jats:italic> < 0.05). Cav-1 interference repressed inflammatory response, reactive oxygen species (ROS) and ICAM-1 levels, and apoptosis in the HUVECs (P<\/jats:italic> < 0.05). Cav-1 messenger RNA was stabilized by HuR, which can bind to the 3\u2019 untranslated region of Cav-1. Increase in HuR level reversed the effects of Cav-1 silencing on ROS and ICAM-1 levels and apoptosis in the HUVECs (P<\/jats:italic> < 0.05). In addition, the levels of inflammatory response, oxidative stress, and atherosclerotic plaque formation induced by P. gingivalis<\/jats:italic> in the mouse model were significantly reduced after Cav-1 expression was inhibited (P<\/jats:italic> < 0.05).<\/jats:p>\n<\/jats:sec>\n\nConclusion:<\/jats:title>\nHuR-activated Cav-1 may promote atherosclerotic plaque formation by modulating inflammatory response and oxidative stress, leading to AS.<\/jats:p>\n<\/jats:sec>","DOI":"10.25259\/cytojournal_76_2024","type":"journal-article","created":{"date-parts":[[2024,11,15]],"date-time":"2024-11-15T12:13:58Z","timestamp":1731672838000},"page":"42","update-policy":"https:\/\/doi.org\/10.25259\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Increased caveolin 1 by human antigen R exacerbates Porphyromonas gingivali<\/i>-induced atherosclerosis by modulating oxidative stress and inflammatory responses"],"prefix":"10.25259","volume":"21","author":[{"given":"Fang","family":"Miao","sequence":"first","affiliation":[{"name":"Department of Prevention and Healthcare, Lanzhou Stomatology Hospital, Lanzhou, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yangyang","family":"Lei","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Second People\u2019s Hospital of Lanzhou City, Lanzhou, China,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yunfei","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Prevention and Healthcare, Lanzhou Stomatology Hospital, Lanzhou, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yongxia","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Second People\u2019s Hospital of Lanzhou City, Lanzhou, China,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ye","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Prevention and Healthcare, Lanzhou Stomatology Hospital, Lanzhou, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Binbin","family":"Jia","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Second People\u2019s Hospital of Lanzhou City, Lanzhou, China,"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"10894","published-online":{"date-parts":[[2024,11,15]]},"reference":[{"key":"10.25259\/Cytojournal_76_2024\/ref-1","doi-asserted-by":"publisher","first-page":"268","DOI":"10.1111\/jcpe.13189","article-title":"Periodontitis and cardiovascular diseases: Consensus report","volume":"47","author":"Sanz","year":"2020","journal-title":"J Clin 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