ArticleJournal of animal science and biotechnology2012
Fibroblast growth factor receptor 3 effects on proliferation and telomerase activity in sheep growth plate chondrocytes.
Article in Journal of animal science and biotechnology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
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- Rapid and simple isolation of precartilaginous stem cells: A novel approach without immunomagnetic bead sorting.Heliyon · 2024Article
- Growing Pains: The Need for Engineered Platforms to Study Growth Plate Biology.Advanced healthcare materials · 2022Review
- Genetics of the phenotypic evolution in sheep: a molecular look at diversity-driving genes.Genetics, selection, evolution : GSE · 2022Review
- Telomerase expression marks transitional growth-associated skeletal progenitor/stem cells.Stem cells (Dayton, Ohio) · 2021Article
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
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- Efficient pathway enrichment and network analysis of GWAS summary data using GSA-SNP2.Nucleic acids research · 2018Article
- The Effect of Botulinum Toxin Type A on Expression Profiling of Long Noncoding RNAs in Human Dermal Fibroblasts.BioMed research international · 2017Article
- Role of Thyroid Hormones in Skeletal Development and Bone Maintenance.Endocrine reviews · 2016Review
- Developmental programming: the role of growth hormone.Journal of animal science and biotechnology · 2015Article
- Comparison of small interfering RNA (siRNA) delivery into bovine monocyte-derived macrophages by transfection and electroporation.Veterinary immunology and immunopathology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelled
backgroundFibroblast growth factor receptor 3 (FGFR3) inhibits growth-plate chondrocyte proliferation and limits bone elongation. Gain-of-function FGFR3 mutations cause dwarfism, reduced telomerase activity and shorter telomeres in growth plate chondroyctes suggesting that FGFR3 reduces proliferative capacity, inhibits telomerase, and enhances senescence. Thyroid hormone (T3) plays a role in cellular maturation of growth plate chondrocytes and a known target of T3 is FGFR3. The present study addressed whether reduced FGFR3 expression enhanced telomerase activity, mRNA expression of telomerase reverse transcriptase (TERT) and RNA component of telomerase (TR), and chondrocyte proliferation, and whether the stimulation of FGFR3 by T3 evoked the opposite response.
resultsSheep growth-plate proliferative zone chondrocytes were cultured and transfected with siRNA to reduce FGFR3 expression; FGFR3 siRNA reduced chondrocyte FGFR3 mRNA and protein resulting in greater proliferation and increased TERT mRNA expression and telomerase activity (p < 0.05). Chondrocytes treated with T3 significantly enhanced FGFR3 mRNA and protein expression and reduced telomerase activity (p < 0.05); TERT and TR were not significantly reduced. The action of T3 at the growth plate may be partially mediated through the FGFR3 pathway.
conclusionsThe results suggest that FGFR3 inhibits chondrocyte proliferation by down-regulating TERT expression and reducing telomerase activity indicating an important role for telomerase in sustaining chondrocyte proliferative capacity during bone elongation.
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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.