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DIFFERENTIAL REGULATION OF GROWTH PLATE CHONDROCYTES BY 1,25-(OH)₂D₃ AND 24R,25-(OH)₂D₃ INVOLVES CELL-MATURATION-SPECIFIC MEMBRANE-RECEPTOR-ACTIVATED PHOSPHOLIPID METABOLISM

¹ Departments of Orthopaedics, ² Periodontics, ³ Biochemistry, and ⁴ Orthodontics, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, MS-7774, San Antonio, TX 78229-3900; and ⁵ Department of Periodontics, Hebrew University Hadassah Faculty of Dental Medicine, Jerusalem, Israel;

View larger version (23K): [in a new window]   Figure 1. Neutral metalloproteinase (MMP) and collagenase content of growth plate cartilage from normal and vitamin D/phosphate-deficient (-VDP) rats. At the animals' death, the proximal tibial growth plate cartilage was removed, and neutral MMP and collagenase were extracted and then assayed on aggrecan and type 1 collagen substrates. All values are the mean ± SEM in enzyme units/gram wet weight tissue for n 7 samples. *P < 0.05, normal vs. –VDP.

View larger version (40K): [in a new window]   Figure 2. Effect of antibody specific for the 1,25-(OH)2D3 membrane receptor (Ab99) on protein kinase C (PKC) activity of growth zone chondrocytes treated with 1,25-(OH)2D3 or analogue 3a. Confluent, fourth-passage growth zone chondrocytes were treated for 9 min with control media, 10-8 M 1,25-(OH)2D3 (left panel) or analogue 3a (right panel) in the absence or presence of Ab99 or rabbit immunoglobulin G1. At harvest, PKC specific activity in the cell layer was determined. Data represent the mean ± SEM of 6 cultures from one of two experiments yielding comparable results. *P < 0.05, treatment vs. control; •p < 0.05, Ab99 vs. no Ab99.

View larger version (41K): [in a new window]   Figure 3. Effect of inhibiting PLC on protein kinase C (PKC) activity in resting zone (RC) and growth zone (GC) chondrocytes. Confluent, fourth-passage RC cells were treated with 10-7 M 24R,25-(OH)2D3 for 90 min (left panel), and GC cells were treated for 9 min with 10-8 M 1,25-(OH)2D3 (right panel) in the presence or absence of the phospholipase C inhibitor U73122 (10 µM). At harvest, PKC specific activity in the cell layer was determined. Data represent the mean ± SEM of 6 cultures from one of two experiments yielding comparable results. *P < 0.05, treatment vs. control; •p < 0.05, U73122 vs. no U73122.

View larger version (41K): [in a new window]   Figure 4. Effect of inhibiting PLD on protein kinase C (PKC) activity in resting zone (RC) and growth zone (GC) chondrocytes. Confluent, fourth-passage RC cells were treated with 10-7 M 24R,25-(OH)2D3 for 90 min (left panel), and GC cells were treated for 9 min with 10-8 M 1,25-(OH)2D3 (right panel) in the presence or absence of the phospholipase D inhibitor wortmannin (10 µM). At harvest, PKC specific activity in the cell layer was determined. Data represent the mean ± SEM of 6 cultures from one of two experiments yielding comparable results. *P < 0.05, treatment vs. control; •p < 0.05, wortmannin vs. no wortmannin.

View larger version (40K): [in a new window]   Figure 5. Effect of activating PLA2 on protein kinase C (PKC) activity in resting zone (RC) and growth zone (GC) chondrocytes. Confluent, fourth-passage RC cells were treated with 10-7 M 24,25-(OH)2D3 for 90 min (left panel), and GC cells were treated for 9 min with 10-8 M 1,25-(OH)2D3 (right panel) in the presence or absence of the phospholipase A2 activator melittin (0.3 µg/mL). At harvest, PKC specific activity in the cell layer was determined. Data represent the mean ± SEM of 6 cultures from one of two experiments yielding comparable results. *P < 0.05, treatment vs. control; •p < 0.05, melittin vs. no melittin.

View larger version (72K): [in a new window]   Figure 6. Mechanism of action of vitamin D3 metabolites. Proposed pathways of action of 1,25-(OH)2D3 in growth zone chondrocytes (GC) and 24,25-(OH)2D3 in resting zone chondrocytes (RC). Phospholipase C (PLC), Phospholipase A2 (PLA2), arachidonic acid (AA), cyclooxygenase-1 (Cox-1), PGE2 EP receptor (EP), phospholipase D (PLD), protein kinase C (PKC), protein kinase A (PKA).