ArticlePLoS genetics2017
Mesoderm-specific Stat3 deletion affects expression of Sox9 yielding Sox9-dependent phenotypes.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Sensing the skeleton: sensorineural regulation in bone.Nature reviews. Neuroscience · 2026Review
- Enhanced neuromorphogenesis of neural stem cells via the optimization of physical stimulus-responsive signaling pathways.Stem cell research & therapy · 2025Article
- STAT3 signaling enhances tissue expansion during postimplantation mouse development.Cell reports · 2025Article
- Contribution of Signal Transducer and Activator of Transcription 3 (STAT3) to Bone Development and Repair.International journal of molecular sciences · 2023Article
- DNA methylation at the suppressor of cytokine signaling 3 (SOCS3) gene influences height in childhood.Nature communications · 2023Article
- Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse.Journal of applied oral science : revista FOB · 2023Article
- Induction of type II collagen expression in M2 macrophages derived from peripheral blood mononuclear cells.Scientific reports · 2022Article
- SOX9 in organogenesis: shared and unique transcriptional functions.Cellular and molecular life sciences : CMLS · 2022Review
- Shikonin Derivatives Inhibit Inflammation Processes and Modulate MAPK Signaling in Human Healthy and Osteoarthritis Chondrocytes.International journal of molecular sciences · 2022Article
- MicroRNA Regulation of Bone Marrow Mesenchymal Stem Cell Chondrogenesis: Toward Articular Cartilage.Tissue engineering. Part A · 2022Article
- gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes.Communications biology · 2022Article
- Skeletal stem cell fate defects caused by Pdgfrb activating mutation.Development (Cambridge, England) · 2021Article
- Loss of signal transducer and activator of transcription 3 impaired the osteogenesis of mesenchymal progenitor cells in vivo and in vitro.Cell & bioscience · 2021Article
- Article
- JAK/STAT Activation: A General Mechanism for Bone Development, Homeostasis, and Regeneration.International journal of molecular sciences · 2020Review
- Histone demethylase LSD1 is critical for endochondral ossification during bone fracture healing.Science advances · 2020Article
- A roadmap to target interleukin-6 in osteoarthritis.Rheumatology (Oxford, England) · 2020Article
- LncRNA MM2P-induced, exosome-mediated transfer of Sox9 from monocyte-derived cells modulates primary chondrocytes.Cell death & disease · 2020Article
- Review
- The JAK1/STAT3/SOCS3 axis in bone development, physiology, and pathology.Experimental & molecular medicine · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
To date, mutations within the coding region and translocations around the SOX9 gene both constitute the majority of genetic lesions underpinning human campomelic dysplasia (CD). While pathological coding-region mutations typically result in a non-functional SOX9 protein, little is known about what mechanism(s) controls normal SOX9 expression, and subsequently, which signaling pathways may be interrupted by alterations occurring around the SOX9 gene. Here, we report the identification of Stat3 as a key modulator of Sox9 expression in nascent cartilage and developing chondrocytes. Stat3 expression is predominant in tissues of mesodermal origin, and its conditional ablation using mesoderm-specific TCre, in vivo, causes dwarfism and skeletal defects characteristic of CD. Specifically, Stat3 loss results in the expansion of growth plate hypertrophic chondrocytes and deregulation of normal endochondral ossification in all bones examined. Conditional deletion of Stat3 with a Sox9Cre driver produces palate and tracheal irregularities similar to those described in Sox9+/- mice. Furthermore, mesodermal deletion of Stat3 causes global embryonic down regulation of Sox9 expression and function in vivo. Mechanistic experiments ex vivo suggest Stat3 can directly activate the expression of Sox9 by binding to its proximal promoter following activation. These findings illuminate a novel role for Stat3 in chondrocytes during skeletal development through modulation of a critical factor, Sox9. Importantly, they further provide the first evidence for the modulation of a gene product other than Sox9 itself which is capable of modeling pathological aspects of CD and underscore a potentially valuable therapeutic target for patients with the disorder.
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Registered trials
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