ArticleDevelopmental biology2009
Retinoic acid receptors are required for skeletal growth, matrix homeostasis and growth plate function in postnatal mouse.
Article in Developmental biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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.
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Who cites it
64 citing papers in PubMed, 98 citations in OpenAlex.
- Temporally regulated FGFR2-retinoic acid signaling mediates dura mater-suture mesenchyme interactions to prevent craniosynostosis in mice.International journal of oral science · 2026Article
- Retinoic Acid Receptor γ Is a Ligand-Activated Gatekeeper to Stem Cell Developmental Progression.International journal of molecular sciences · 2026Review
- The role of RARG in solid tumor progression and therapeutic potential.Discover oncology · 2026Review
- The Influences of RARγ on the Behavior of Normal and Cancer Stem Cells.International journal of molecular sciences · 2026Review
- Sex- and age-specific musculoskeletal adverse events of isotretinoin: disproportionality analysis of the FAERS database combined with a clinical case series.Frontiers in pharmacology · 2026Article
- A Retinoid Antagonist Attenuates Bone Growth Inhibition Caused by Growth Plate Injury in Mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Synovial joint cavitation during limb skeletogenesis entails Na/K-ATPase ion pump expression and osmoregulatory activity.Development (Cambridge, England) · 2025Article
- Retinoid-impregnated nanoparticles enable control of bone growth by site-specific modulation of endochondral ossification in mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Article
- Review
- Analysis of the Actions of RARγ Agonists on Growing Osteochondromas in a Mouse Model.International journal of molecular sciences · 2024Article
- Whole-genome resequencing reveals genomic variation and dynamics in Ethiopian indigenous goats.Frontiers in genetics · 2024Article
- Cytochrome P450 enzymes in the black-spotted frog (Frontiers in physiology · 2024Article
- Spatiotemporal Characterization of Human Early Intervertebral Disc Formation at Single-Cell Resolution.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Direct Reprogramming of Mouse Subchondral Bone Osteoblasts into Chondrocyte-like Cells.Biomedicines · 2022Article
- Synthetic Retinoids Beyond Cancer Therapy.Annual review of pharmacology and toxicology · 2022Review
- Retinoic Acid Receptor Gamma (RARMediators of inflammation · 2022Article
- Selective Retinoic Acid Receptor γ Antagonist 7C is a Potent Enhancer of BMP-Induced Ectopic Endochondral Bone Formation.Frontiers in cell and developmental biology · 2022Article
- Osteochondroma Pathogenesis: Mouse Models and Mechanistic Insights into Interactions with Retinoid Signaling.The American journal of pathology · 2021Review
- Review
- Transcriptional profiling of mESC-derived tendon and fibrocartilage cell fate switch.Nature communications · 2021Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
The retinoic acid receptors alpha, beta and gamma (RARalpha, RARbeta and RARgamma) are nuclear hormone receptors that regulate fundamental processes during embryogenesis, but their roles in skeletal development and growth remain unclear. To study skeletal-specific RAR function, we created conditional mouse mutants deficient in RAR expression in cartilage. We find that mice deficient in RARalpha and RARgamma (or RARbeta and RARgamma) exhibit severe growth retardation obvious by about 3 weeks postnatally. Their growth plates are defective and, importantly, display a major drop in aggrecan expression and content. Mice deficient in RARalpha and RARbeta, however, are virtually normal, suggesting that RARgamma is essential. In good correlation, we find that RARgamma is the most strongly expressed RAR in mouse growth plate and its expression characterizes the proliferative and pre-hypertrophic zones where aggrecan is strongly expressed also. By being avascular, those zones lack endogenous retinoids as indicated by previous RARE reporter mice and our direct biochemical measurements and thus, RARgamma is likely to exert ligand-less repressor function. Indeed, our data indicate that: aggrecan production is enhanced by RARgamma over-expression in chondrocytes under retinoid-free culture conditions; production is further boosted by co-repressor Zac1 or pharmacologic agents that enhance RAR repressor function; and RAR/Zac1 function on aggrecan expression may involve Sox proteins. In sum, our data reveal that RARs, and RARgamma in particular, exert previously unappreciated roles in growth plate function and skeletal growth and regulate aggrecan expression and content. Since aggrecan is critical for growth plate function, its deficiency in RAR-mutant mice is likely to have contributed directly to their growth retardation.
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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.