{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T20:35:50Z","timestamp":1777667750704,"version":"3.51.4"},"reference-count":33,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2015,1,30]],"date-time":"2015-01-30T00:00:00Z","timestamp":1422576000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Hum Exp Toxicol"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:p>\n                    Naproxen is an anti-inflammatory drug that affects cellular calcium ion (Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ) homeostasis and viability in different cells. This study explored the effect of naproxen on [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    and viability in Madin-Darby canine kidney cells (MDCK) canine renal tubular cells. At concentrations between 50 \u03bcM and 300 \u03bcM, naproxen induced [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    rises in a concentration-dependent manner. This Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signal was reduced partly when extracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    was removed. The Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signal was inhibited by a Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channel blocker nifedipine but not by store-operated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channel inhibitors (econazole and SKF96365), a protein kinase C (PKC) activator phorbol 12-myristate 13-acetate, and a PKC inhibitor GF109203X. In Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -free medium, pretreatment with 2,5-di-tert-butylhydroquinone or thapsigargin, an inhibitor of endoplasmic reticulum Ca\n                    <jats:sup>2+<\/jats:sup>\n                    pumps, partly inhibited naproxen-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signal. Inhibition of phospholipase C with U73122 did not alter naproxen-evoked [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    rises. At concentrations between 15 \u03bcM and 30 \u03bcM, naproxen killed cells in a concentration-dependent manner, which was not reversed by prechelating cytosolic Ca\n                    <jats:sup>2+<\/jats:sup>\n                    with the acetoxymethyl ester of 1,2-bis(2-aminophenoxy)ethane- N, N, N\u2032, N\u2032-tetraacetic acid acetoxymethyl. Annexin V\/propidium iodide staining data suggest that naproxen induced apoptosis. Together, in MDCK renal tubular cells, naproxen induced [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    rises by inducing Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release from multiple stores that included the endoplasmic reticulum and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry via nifedipine-sensitive Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channels. Naproxen induced cell death that involved apoptosis.\n                  <\/jats:p>","DOI":"10.1177\/0960327115569810","type":"journal-article","created":{"date-parts":[[2015,1,31]],"date-time":"2015-01-31T00:17:17Z","timestamp":1422663437000},"page":"1096-1105","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Naproxen-induced Ca\n                    <sup>2+<\/sup>\n                    movement and death in MDCK canine renal tubular cells"],"prefix":"10.1177","volume":"34","author":[{"given":"H-H","family":"Cheng","sequence":"first","affiliation":[{"name":"Department of Medicine, Chang Bing Show Chwan Memorial Hospital, Changhua County, Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C-T","family":"Chou","sequence":"additional","affiliation":[{"name":"Department of Nursing, Division of Basic Medical Sciences, Chang Gung Institute of Technology, Chia-Yi, Taiwan"},{"name":"Chronic 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Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H-W","family":"Tseng","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C-C","family":"Kuo","sequence":"additional","affiliation":[{"name":"Department of Nursing, Tzu Hui Institute of Technology, Pingtung, Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F-A","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Tajen University, Pingtung, Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D-H","family":"Kuo","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Tajen University, Pingtung, Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P","family":"Shieh","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Tajen University, Pingtung, 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