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Effects of 1,25-Dihydroxyvitamin D₃ and Growth Hormone on Apoptosis and Proliferation in UMR 106 Osteoblast-Like Cells

Center for Surgical Sciences (O.M., M.K.R.S., U.L.), Division of Orthopedics, Karolinska Institutet, Huddinge University Hospital, S-141 86 Huddinge, Sweden; and Department of Medical Nutrition (L.-A.H.), Karolinska Institutet, Novum, S-141 86 Huddinge, Sweden

Address all correspondence and requests for reprints to: Lars-Arne Haldosén, Department of Medical Nutrition, Karolinska Institutet, Novum, S-141 86 Huddinge, Sweden. E-mail: lars-arne.haldosen{at}mednut.ki.se.

Mechanisms maintaining a correct balance between bone-forming osteoblasts and bone-resorbing osteoclasts are essential for bone formation. Apoptosis has been proposed to play a key role in controlling osteoblast homeostasis. 1,25-dihydroxyvitamin D3 [1,25(OH)₂D₃] and GH, which are important regulators of bone growth and bone metabolism, also play pivotal roles in regulation of mitogenesis, differentiation, and apoptosis. We have recently shown that 1,25(OH)₂D₃ prolongs GH signaling via the Janus kinase 2 (JAK2)/STAT5 (signal transducer and activator of transcription 5) pathway in UMR 106 osteoblast-like cells. In the present study, we have investigated the effects of GH and 1,25(OH)₂D₃ on proliferation and apoptosis in UMR 106 cells. We found that 1,25(OH)₂D₃ and GH, separate or in combination, inhibited apoptosis. GH also had profound effects on cell cycle distribution and proliferation. In addition, pretreatment of cells with 1,25(OH)₂D₃ was necessary to detect GH-induced MAPK activation. We hypothesize that these hormones separately regulate the processes of apoptosis and proliferation, which may be important for maintaining osteoblast cell number.

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