ArticleMolecular and cellular endocrinology2018
Deletion of protein kinase D1 in osteoprogenitor cells results in decreased osteogenesis in vitro and reduced bone mineral density in vivo.
Article in Molecular and cellular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Genes involved in osteogenic differentiation induced by low‑intensity pulsed ultrasound in goldfish scales.Biomedical reports · 2025Article
- Prkd1 regulates the formation and repair of plasma membrane disruptions (PMD) in osteocytes.Bone · 2024Article
- Effect of deletion of the protein kinase PRKD1 on development of the mouse embryonic heart.Journal of anatomy · 2024Article
- Genome-wide association study implicates novel loci and reveals candidate effector genes for longitudinal pediatric bone accrual.Genome biology · 2021Article
- Protein kinase D1 conditional null mice show minimal bone loss following ovariectomy.Molecular and cellular endocrinology · 2018Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Protein kinase D1 (PRKD1) is thought to play a role in a number of cellular functions, including proliferation and differentiation. We hypothesized that PRKD1 in bone marrow-derived mesenchymal stem cells (BMMSC) could modulate osteogenesis. In BMMSCs from floxed PRKD1 mice, PRKD1 ablation with adenovirus-mediated Cre-recombinase expression inhibited BMMSC differentiation in vitro. In 3- and 6-month-old conditional knockout mice (cKO), in which PRKD1 was ablated in osteoprogenitor cells by osterix promoter-driven Cre-recombinase, bone mineral density (BMD) was significantly reduced compared with floxed control littermates. Microcomputed tomography analysis also demonstrated a decrease in trabecular thickness and bone volume fraction in cKO mice at these ages. Dynamic bone histomorphometry suggested a mineralization defect in the cKO mice. However, by 9 months of age, the bone appeared to compensate for the lack of PRKD1, and BMD was not different. Taken together, these results suggest a potentially important role for PRKD1 in bone formation.
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Registered trials
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