ArticleScientific reports2024
Noggin promotes osteogenesis in human adipose-derived mesenchymal stem cells via FGFR2/Src/Akt and ERK signaling pathway.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Understanding of the different roles of Noggin in the Noggin-BMP-2 and Noggin-BMP-9 dimer complexes at the molecular level.Scientific reports · 2026Article
- The Interplay of Angiogenesis and Osteogenesis in Non-Stabilized Incomplete Tibial Fractures: A Temporal Study in Rats.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Rapid osteoinduction of human adipose-derived stem cells grown on bioactive surfaces and stimulated by chemically modified media flow.Journal of biological engineering · 2025Article
- Novel Strategies for Spatiotemporal and Controlled BMP-2 Delivery in Bone Tissue Engineering.Cell transplantationReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The balance between Noggin and bone morphogenetic proteins (BMPs) is important during early development and skeletal regenerative therapies. Noggin binds BMPs in the extracellular space, thereby preventing BMP signaling. However, Noggin may affect cell response not necessarily through the modulation of BMP signaling, raising the possibility of direct Noggin signaling through yet unspecified receptors. Here we show that in osteogenic cultures of adipose-derived stem cells (ASCs), Noggin activates fibroblast growth factor receptors (FGFRs), Src/Akt and ERK kinases, and it stabilizes TAZ proteins in the presence of dexamethasone. Overall, this leads ASCs to increased expression of osteogenic markers and robust mineral deposition. Our results also indicate that Noggin can induce osteogenic genes expression in normal human bone marrow stem cells and alkaline phosphatase activity in normal human dental pulp stem cells. Besides, Noggin can specifically activate FGFR2 in osteosarcoma cells. We believe our findings open new research avenues to further explore the involvement of Noggin in cell fate modulation by FGFR2/Src/Akt/ERK signaling and potential applications of Noggin in bone regenerative therapies.
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Registered trials
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