ArticleDevelopment (Cambridge, England)2021
Skeletal stem cell fate defects caused by Pdgfrb activating mutation.
Article in Development (Cambridge, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Hyperactive PDGFRβ signaling induces cataractogenesis via TGFβ and STAT5-IGF1.Developmental biology · 2025Article
- Mouse scalp development requires Rac1 and SRF for the maintenance of mechanoresponsive mesenchyme.Development (Cambridge, England) · 2025Article
- 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
- Skeletal stem and progenitor cells in bone physiology, ageing and disease.Nature reviews. Endocrinology · 2025Review
- Sclerostin blockade inhibits bone resorption through PDGF receptor signaling in osteoblast lineage cells.JCI insight · 2024Article
- Mild photothermal therapy assist in promoting bone repair: Related mechanism and materials.Materials today. Bio · 2023Review
- PROX1 Inhibits PDGF-B Expression to Prevent Myxomatous Degeneration of Heart Valves.Circulation research · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Autosomal dominant PDGFRβ gain-of-function mutations in mice and humans cause a spectrum of wasting and overgrowth disorders afflicting the skeleton and other connective tissues, but the cellular origin of these disorders remains unknown. We demonstrate that skeletal stem cells (SSCs) isolated from mice with a gain-of-function D849V point mutation in PDGFRβ exhibit colony formation defects that parallel the wasting or overgrowth phenotypes of the mice. Single-cell RNA transcriptomics with SSC-derived polyclonal colonies demonstrates alterations in osteogenic and chondrogenic precursors caused by PDGFRβD849V. Mutant cells undergo poor osteogenesis in vitro with increased expression of Sox9 and other chondrogenic markers. Mice with PDGFRβD849V exhibit osteopenia. Increased STAT5 phosphorylation and overexpression of Igf1 and Socs2 in PDGFRβD849V cells suggests that overgrowth in mice involves PDGFRβD849V activating the STAT5-IGF1 axis locally in the skeleton. Our study establishes that PDGFRβD849V causes osteopenic skeletal phenotypes that are associated with intrinsic changes in SSCs, promoting chondrogenesis over osteogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.