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pubmed:abstractText |
Experimental cutaneous calcification was induced by a subcutaneous injection of lead acetate in parathyroidectomized (PTX) rats and vitamin D-deficient rats whose plasma calcium concentrations were controlled by diets containing various amounts of calcium. Although, in PTX rats, the calcium content of the calcified plaque induced by lead acetate was correlated with their plasma calcium concentration, calcium content of the calcified plaque in vitamin D-deficient rats with normocalcemia was significantly lower than those in control and PTX rats with normocalcemia. A subcutaneous administration of 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3) following the lead acetate injection increased calcium content of the calcified plaque in vitamin D-deficient mice, suggesting the involvement of vitamin D in the cutaneous calcification. As the synthesis of osteocalcin, osteopontin and interleukin-1 (IL-1) receptor is well known to be increased by 1 alpha,25(OH)2D3, gene expressions of mRNAs of these proteins were examined in the skin with calcified plaque by reverse transcription polymerase chain reaction (RT-PCR) analysis. These mRNA expressions in the skin with calcified plaque were increased by a subcutaneous administration of 1 alpha,25(OH)2D3 following the lead acetate injection. On the contrary, they decreased in vitamin D-deficient mice. These findings suggest that vitamin D is directly involved in the process of experimental calcification.
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