{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T02:52:18Z","timestamp":1774579938394,"version":"3.50.1"},"reference-count":47,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2010,7,27]],"date-time":"2010-07-27T00:00:00Z","timestamp":1280188800000},"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":[[2010,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Vitamin D sterol administration, a traditional treatment for secondary hyperparathyroidism, may increase serum calcium and phosphorus, and has been associated with increased vascular calcification (VC). In vitro studies suggest that in the presence of uremic concentrations of phosphorus, vitamin D sterols regulate gene expression associated with trans\u2010differentiation of smooth muscle cells (SMCs) to a chondro\/osteoblastic cell type. This study examined effects of vitamin D sterols on gene expression profiles associated with phosphate\u2010enhanced human coronary artery SMC (CASMC) calcification. Cultured CASMCs were exposed to phosphate\u2010containing differentiation medium (DM) with and without calcitriol, paricalcitol, or the calcimimetic R\u2010568 (10<jats:sup>\u221211<\/jats:sup>\u201310<jats:sup>\u22127<\/jats:sup>\u2009M) for 7 days. Calcification of CASMCs, determined using colorimetry following acid extraction, was dose dependently increased (1.6\u2010 to 1.9\u2010fold) by vitamin D sterols\u2009+\u2009DM. In contrast, R\u2010568 did not increase calcification. Microarray analysis demonstrated that, compared with DM, calcitriol (10<jats:sup>\u22128<\/jats:sup>\u2009M)\u2009+\u2009DM or paricalcitol (10<jats:sup>\u22128<\/jats:sup>\u2009M)\u2009+\u2009DM similarly and significantly (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05) regulated genes of various pathways including: metabolism, CYP24A1; mineralization, ENPP1; apoptosis, GIP3; osteo\/chondrogenesis, OPG, TGFB2, Dkk1, BMP4, BMP6; cardiovascular, HGF, DSP1, TNC; cell cycle, MAPK13; and ion channels, SLC22A3 KCNK3. R\u2010568 had no effect on CASMC gene expression. Thus, SMC calcification observed in response to vitamin D sterol\u2009+\u2009DM may be partially mediated through targeting mineralization, apoptotic, osteo\/chondrocytic, and cardiovascular pathway genes, although some gene changes may protect against calcification. Further studies to determine precise roles of these genes in development of, or protection against VC and cardiovascular disease are required. J. Cell. Biochem. 111: 911\u2013921, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.22779","type":"journal-article","created":{"date-parts":[[2010,7,27]],"date-time":"2010-07-27T14:58:41Z","timestamp":1280242721000},"page":"911-921","source":"Crossref","is-referenced-by-count":29,"title":["Chondro\/osteoblastic and cardiovascular gene modulation in human artery smooth muscle cells that calcify in the presence of phosphate and calcitriol or 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