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This review discusses the regulation of growth plate chondrocytes by vitamin D 3 . Over the past ten years, our understanding of how two vitamin D metabolites, 1α,25-(OH) 2 D 3  and 24R,25-(OH) 2 D 3 , exert their effects on endochondral ossification has undergone considerable advances through the use of cell biology and signal transduction methodologies. These studies have shown that each metabolite affects a primary target cell within the endochondral developmental lineage. 1α,25-(OH) 2 D 3  affects primarily growth zone cells, and 24R,25-(OH) 2 D 3  affects primarily resting zone cells. In addition, 24R,25-(OH) 2 D 3  initiates a differentiation cascade that results in down-regulation of responsiveness to 24R,25-(OH) 2 D 3  and up-regulation of responsiveness to 1α,25-(OH) 2 D 3 . 1α,25-(OH) 2 D 3  regulates growth zone chondrocytes both through the nuclear vitamin D receptor, and through a membrane-associated receptor that mediates its effects via a protein kinase C (PKC) signal transduction pathway. PKCα is increased via a phosphatidylinositol-specific phospholipase C (PLC)-dependent mechanism, as well as through the stimulation of phospholipase A 2  (PLA 2 ) activity. Arachidonic acid and its downstream metabolite prostaglandin E 2  (PGE 2 ) also modulate cell response to 1α,25-(OH) 2 D 3 . In contrast, 24R,25-(OH) 2 D 3  exerts its effects on resting zone cells through a separate, membrane-associated receptor that also involves PKC pathways. PKCα is increased via a phospholipase D (PLD)-mediated mechanism, as well as through inhibition of the PLA 2  pathway. The target-cell-specific effects of each metabolite are also seen in the regulation of matrix vesicles by vitamin D 3 . However, the PKC isoform involved is PKCζ, and its activity is inhibited, providing a mechanism for differential autocrine regulation of the cell and events in the matrix by these two vitamin D 3  metabolites.

critical reviews in oral biology and medicine

D<scp>ifferential</scp>R<scp>egulation of</scp>G<scp>rowth</scp>P<scp>late</scp>C<scp>hondrocytes by</scp>1α,25-(OH)2D3<scp>and</scp>24R,25-(OH)2D3I<scp>nvolves</scp>C<scp>ell-maturation-specific</scp>M<scp>embrane-receptor-activated</scp>P<scp>hospholipid</scp>M<scp>etabolism</scp>

DifferentialRegulation ofGrowthPlateChondrocytes by1α,25-(OH)2D3and24R,25-(OH)2D3InvolvesCell-maturation-specificMembrane-receptor-activatedPhospholipidMetabolism

DifferentialRegulation ofGrowthPlateChondrocytes by1α,25-(OH)₂D₃and24R,25-(OH)₂D₃InvolvesCell-maturation-specificMembrane-receptor-activatedPhospholipidMetabolism