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      1,25-Dihydroxyvitamin D 3 Stimulates Osteopontin Expression in Rat Kidney

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          Osteopontin (OPN) is a secreted phosphoprotein expressed constitutively in the descending thin limb (DTL) and papillary surface epithelium (PSE) of the kidney. Although its function is not fully established, a role for OPN in the regulation of calcium-mediated or calcium-dependent processes has been proposed. The aim of this study was to examine the effects of 1,25-dihydroxyvitamin D<sub>3</sub> (vitD), a hormone involved in the regulation of calcium homeostasis, on renal OPN expression. Four groups of rats were studied: acute vehicle (single intraperitoneal [i.p.] injection of 0.1 ml 10% ethanol-90% propylene glycol, 12 h before being killed); acute vitD (single injection of vitD, 2 ng/g i.p., 12 h before being killed); chronic vehicle (daily subcutaneous [s.c.] injection of 0.1 ml 10% ethanol-90% propylene glycol for 7 days); and chronic vitD (daily s.c. injection of vitD, 0.5 ng/g, for 7 days). Kidneys were processed for light and electron microscope immunocytochemistry, in situ hybridization, and Western blot analysis. In vehicle-treated animals, OPN mRNA and protein were expressed primarily in the DTL and PSE. In the acute vitD group, OPN mRNA and immunoreactivity appeared in the thick ascending limb (TAL) of the inner stripe of the outer medulla, and increased slightly in the DTL and PSE. The proximal tubules exhibited strong OPN immunoreactivity, but no hybridization signal. In the chronic vitD group, there was a marked increase in OPN mRNA and immunoreactivity in the distal tubule, including the TAL, as well as in the DTL and PSE. A weak hybridization signal and immunostaining were also observed in some proximal tubules. Administration of vitD causes a marked increase in OPN mRNA and protein in the rat kidney, mainly in the distal nephron, but also in the DTL, PSE, and proximal tubules. These results indicate that vitD is involved in the regulation of OPN expression in the kidney.

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          Expression, roles, receptors, and regulation of osteopontin in the kidney.

          Osteopontin (OPN) is a secreted glycoprotein in both phosphorylated and non-phosphorylated forms. It contains an Arg-Gly-Asp cell-binding sequence and a thrombin-cleavage site. OPN is mainly present in the loop of Henle and distal nephrons in normal kidneys in animals and humans. After renal damage, OPN expression may be significantly up-regulated in all tubule segments and glomeruli. Studies utilizing OPN gene-deficient mice, antisense-treated or anti-OPN-treated animals have demonstrated that OPN promotes accumulation of macrophages, and may play a role in macrophage-mediated renal injury, but that the effect may be mild and short-lived. On the other hand, OPN has some renoprotective actions in renal injury, such as increasing tolerance to acute ischemia, inhibiting inducible nitric oxide synthase and suppressing nitric oxide synthesis, reducing cell peroxide levels and promoting the survival of cells exposed to hypoxia, decreasing cell apoptosis and participating in the regeneration of cells. In addition, OPN is associated with renal stones, but whether it acts as a promoter or inhibitor of stone formation is controversial. It has been demonstrated that OPN receptors include two families: integrin and CD44. The OPN integrin receptors include alpha(v)beta(3), alpha(v)beta(1), alpha(v)beta(5) and alpha(9)beta(1), and alpha(4)beta(1). In normal human kidneys, standard CD44 is expressed most dominantly. Different OPN functions are mediated via distinct receptors. Parathyroid hormone, vitamin D(3), calcium, phosphate and some cytokines increase OPN expression in vitro or in vivo, whereas female sex hormones and angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists decrease OPN expression in some renal damage states.
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            Interleukin 1 regulates the expression of osteopontin mRNA by osteoblasts


              Author and article information

              Nephron Physiol
              Nephron Physiology
              S. Karger AG
              March 2003
              31 March 2003
              : 93
              : 3
              : p76-p86
              aDepartment of Anatomy and Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Seoul, and bDepartment of Internal Medicine, Sungkyunkwan University, Seoul, Korea; cDepartment of Medicine, University of Florida, Gainesville, Fla., USA
              69556 Nephron Physiol 2003;93:p76–p86
              © 2003 S. Karger AG, Basel

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              Page count
              Figures: 6, Tables: 1, References: 40, Pages: 1
              Self URI (application/pdf):
              Original Paper

              Cardiovascular Medicine, Nephrology

              Rat kidney, Osteopontin, Vitamin D, Calcium


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