Parathyroid Hormone and Transforming Growth Factor-β1 Coregulate Chondrocyte Differentiation In Vitro
| Autor: | David D Dean, Zvi Schwartz, E. Nasatzky, Barbara D. Boyan, E. Azran |
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| Rok vydání: | 2000 |
| Předmět: |
Male
medicine.medical_specialty Endocrinology Diabetes and Metabolism Parathyroid hormone Stimulation Sulfur Radioisotopes Tritium Chondrocyte Rats Sprague-Dawley Chondrocytes Endocrinology Transforming Growth Factor beta Internal medicine medicine Animals Cells Cultured Dose-Response Relationship Drug Sulfates Chemistry Cell Differentiation Drug Synergism DNA Alkaline Phosphatase In vitro Rats medicine.anatomical_structure Parathyroid Hormone Cell culture Alkaline phosphatase Signal transduction Signal Transduction Transforming growth factor |
| Zdroj: | Endocrine. 13:305-313 |
| ISSN: | 0969-711X |
| DOI: | 10.1385/endo:13:3:305 |
| Popis: | Parathyroid hormone (1-34) (PTH(1-34) and transforming growth factor-beta1 (TGF-beta1) regulate chondrocyte proliferation, differentiation, and matrix synthesis. Both proteins mediate their effects in a dose- and time-dependent manner, and the effects are cell maturation specific. Moreover, similar signaling pathways are used, suggesting that there may be cross talk leading to coregulated cell response. To test this hypothesis, confluent cultures of rat costochondral resting zone and growth zone chondrocytes were treated with 0.22, 0.44, or 0.88 ng/mL of rhTGF-beta1 for 24 h, followed by treatment with 10(-11) to 10(-8) M PTH(1-34) for 10 min or 24 h. [3H]-Thymidine incorporation, specific activity of alkaline phosphatase (AP), and [35S]-sulfate incorporation were measured. PTH(1-34) had no effect on [3H]-thymidine incorporation by growth zone cells pretreated with 0.22 or 0.44 ng/mL of TGF-beta1, but in cultures treated with 0.88 ng/mL, PTH(1-34) caused a dose-dependent decrease that was maximal at the lowest concentration tested. By contrast, PTH(1-34) stimulated [3H]-thymidine incorporation by resting zone cells, and this effect was additive with the stimulation caused by 0.22 ng/mL of TGF-beta1. PTH(1-34) caused a synergistic increase in AP in growth zone cells treated with 0.44 or 0.88 ng/mL of TGF-beta1, but not in cells treated with 0.22 ng/mL of TGF-beta1. It had no effect on AP in resting zone cells pretreated with any concentration of TGF-beta1. PTH(1-34) increased [35S]-sulfate incorporation in growth zone and resting zone cell cultures treated with 0.22 ng/mL of TGF-beta1 to levels seen in cultures treated with 0.88 ng/mL of TGF-beta1 alone. These results support the hypothesis that PTH(1-34) and TGF-beta1 coregulate growth plate chondrocytes and that the effects are cell maturation dependent. |
| Databáze: | OpenAIRE |
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