Protein kinase D3 conditional knockout impairs osteoclast formation and increases trabecular bone volume in male mice

Burciaga, Samuel D.; Saavedra, Flávia; Fischer, Lori A.; Johnstone, Karen F.; Jensen, Eric D.

doi:10.1016/j.bone.2023.116759

Cited by 2 publications

(2 citation statements)

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“…PRKD3 belonged to the serine/threonine protein kinase D family and could bind to diacylglycerol and phorbol lipids, playing critical roles in protein transport, cell migration, proliferation, and epithelial-mesenchymalization [ 35 ]. Studies showed that PRKD3 was the major form of PRKD in osteoclasts [ 36 ]. Activation of PRKD3 enhanced osteoclast activity, while inhibitors of PRKD3 hindered the differentiation and motility of multinucleated mature osteoclasts [ 20 ], and increased trabecular bone volume [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

“…Studies showed that PRKD3 was the major form of PRKD in osteoclasts [ 36 ]. Activation of PRKD3 enhanced osteoclast activity, while inhibitors of PRKD3 hindered the differentiation and motility of multinucleated mature osteoclasts [ 20 ], and increased trabecular bone volume [ 36 ]. Furthermore, PRKD3 promoted cartilage destruction by modulating the expression of FOS/JUN and the production of pro-inflammatory MMP1/13 [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

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CircPRKD3/miR-6783-3p responds to mechanical force to facilitate the osteogenesis of stretched periodontal ligament stem cells

Liu,

Wang

et al. 2024

J Orthop Surg Res

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Background The mechanotransduction mechanisms by which cells regulate tissue remodeling are not fully deciphered. Circular RNAs (circRNAs) are crucial to various physiological processes, including cell cycle, differentiation, and polarization. However, the effects of mechanical force on circRNAs and the role of circRNAs in the mechanobiology of differentiation and remodeling in stretched periodontal ligament stem cells (PDLSCs) remain unclear. This article aims to explore the osteogenic function of mechanically sensitive circular RNA protein kinase D3 (circPRKD3) and elucidate its underlying mechanotransduction mechanism. Materials and methods PDLSCs were elongated with 8% stretch at 0.5 Hz for 24 h using the Flexcell® FX-6000™ Tension System. CircPRKD3 was knockdown or overexpressed with lentiviral constructs or plasmids. The downstream molecules of circPRKD3 were predicted by bioinformatics analysis. The osteogenic effect of related molecules was evaluated by quantitative real-time PCR (qRT‐PCR) and western blot. Results Mechanical force enhanced the osteogenesis of PDLSCs and increased the expression of circPRKD3. Knockdown of circPRKD3 hindered PDLSCs from osteogenesis under mechanical force, while overexpression of circPRKD3 promoted the early osteogenesis process of PDLSCs. With bioinformatics analysis and multiple software predictions, we identified hsa-miR-6783-3p could act as the sponge of circPRKD3 to indirectly regulate osteogenic differentiation of mechanically stimulated PDLSCs. Conclusions Our results first suggested that both circPRKD3 and hsa-miR-6783-3p could enhance osteogenesis of stretched PDLSCs. Furthermore, hsa-miR-6783-3p could sponge circPRKD3 to indirectly regulate RUNX2 during the periodontal tissue remodeling process in orthodontic treatment.

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Section: Discussionmentioning

confidence: 99%