Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 18, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/ijms18102221
Keywords
human mesenchymal stem cells; osteogenesis; parathyroid hormone; PKC delta
Funding
- Ministry of Science and Technology, Taiwan [MOST103-2314-B-010-053-MY3, MOST 106-2321-B-010-008, MOST 106-2911-I-010-502, MOST 106-3114-B-010-002]
- Aiming for the Top University Plan, a grant from Ministry of Education
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Human mesenchymal stem cells (hMSCs) can differentiate into osteoblasts and are regulated by chemical cues. The recombinant N-terminal (1-34 amino acids) fragment of the parathyroid hormone (PTH (1-34)) is identified to promote osteogenesis. The osteoanabolic effects of intermittent PTH (1-34) treatment are linked to a complex consisting of signaling pathways; additionally, protein kinase C (PKC) act as mediators of multifunctional signaling transduction pathways, but the role of PKC delta (PKC delta), a downstream target in regulating osteoblast differentiation during intermittent administration of PTH (1-34) is less studied and still remains elusive. The purpose of this study is to examine the role of PKC delta during intermittent and continuous PTH (1-34) administration using osteoblast-lineage-committed hMSCs. Relative gene expression of osteoblast-specific genes demonstrated significant upregulation of RUNX2, type I Collagen, ALP, and Osterix and increased alkaline phosphatase activity in the presence of PTH (1-34). Intermittent PTH (1-34) administration increased PKC activity at day 7 of osteogenic differentiation, whereas inhibition of PKC activity attenuated these effects. In addition, the specific isoform PKC delta was activated upon treatment. These findings demonstrate that intermittent PTH (1-34) treatment enhances the osteogenesis of hMSCs by upregulating osteoblast-specific genes via PKC delta activation.
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