{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:38:11Z","timestamp":1761896291628,"version":"3.37.3"},"reference-count":39,"publisher":"Wiley","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003621","name":"Ministry of Science, ICT and Future Planning","doi-asserted-by":"publisher","award":["2014R1A1A3049477","NRF-2015K2A1A2069479"],"award-info":[{"award-number":["2014R1A1A3049477","NRF-2015K2A1A2069479"]}],"id":[{"id":"10.13039\/501100003621","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea","doi-asserted-by":"publisher","award":["2014R1A1A3049477","NRF-2015K2A1A2069479"],"award-info":[{"award-number":["2014R1A1A3049477","NRF-2015K2A1A2069479"]}],"id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2016]]},"abstract":"<jats:p>Exposure to bacterial lipopolysaccharides (LPS) induces inflammatory signals in salivary glands. We investigated the regulatory role of phosphodiesterase 4 (PDE4) inhibitor rolipram on inflammatory mediators and cholinergic\/adrenergic stimulation-induced intracellular Ca<jats:sup>2+<\/jats:sup>signaling in salivary acinar and ductal cells. Submandibular gland (SMG) expressed PDE4A through 4D mRNA and PDE4 was localized in the luminal membrane of SMG. LPS induced Ca<jats:sup>2+<\/jats:sup>signaling and ROS production in SMG. Treatment with rolipram blocked LPS-induced Ca<jats:sup>2+<\/jats:sup>increase and ROS production. The application of histamine evoked Ca<jats:sup>2+<\/jats:sup>signals and ROS production, which were attenuated by rolipram in SMG cells. Moreover, LPS-induced NLRP3 inflammasome and cleaved caspase-1 were inhibited by rolipram. The inhibitory role of rolipram in ROS-induced Ca<jats:sup>2+<\/jats:sup>signaling was mainly observed in acinar cells and not in ductal cells. Rolipram also protected SMG acinar but not ductal cells from LPS-induced cell membrane damage. In the case of cholinergic\/adrenergic stimulation, carbachol\/isoproterenol-induced Ca<jats:sup>2+<\/jats:sup>signals were upregulated by the treatment of rolipram in SMG. In the case of cAMP-dependent ductal bicarbonate secretion by rolipram, no effect was observed on the modulation of ductal chloride\/bicarbonate exchange activity. Rolipram could suppress the inflammatory signals and could be a potential therapeutic strategy against LPS-induced inflammation to protect the salivary gland cells.<\/jats:p>","DOI":"10.1155\/2016\/3745961","type":"journal-article","created":{"date-parts":[[2016,4,8]],"date-time":"2016-04-08T07:29:46Z","timestamp":1460100586000},"page":"1-11","source":"Crossref","is-referenced-by-count":15,"title":["The Regulatory Role of Rolipram on Inflammatory Mediators and Cholinergic\/Adrenergic Stimulation-Induced Signals in Isolated Primary Mouse Submandibular Gland Cells"],"prefix":"10.1155","volume":"2016","author":[{"given":"Dong Un","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine, Gachon University, 191 Hambakmeoro, Yeonsu-gu, Incheon 406-799, Republic of Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dong Min","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Oral Biology, BK21 PLUS 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