ArticleDevelopmental cell2012
FoxA family members are crucial regulators of the hypertrophic chondrocyte differentiation program.
Article in Developmental cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 88 citations in OpenAlex.
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- Downregulation of Nesprin1 by Runx2 deficiency is critical for the development of skeletal laminopathy-like pathology.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Innate immune pathway activation to modulate mesenchymal stromal cell (MSC) interactions with synovium and cartilage.Frontiers in bioengineering and biotechnology · 2025Article
- Modeling of skeletal development and diseases using human pluripotent stem cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Review
- FOXC1 and FOXC2 regulate growth plate chondrocyte maturation towards hypertrophy in the embryonic mouse limb skeleton.Development (Cambridge, England) · 2024Article
- Getting to the Core: Exploring the Embryonic Development from Notochord to Nucleus Pulposus.Journal of developmental biology · 2024Review
- Pre-hypertrophic chondrogenic enhancer landscape of limb and axial skeleton development.Nature communications · 2024Article
- Article
- Hypertrophic chondrocytes at the junction of musculoskeletal structures.Bone reports · 2023Article
- Runt-related Transcription Factors and Gene Regulatory Mechanisms in Skeletal Development and Diseases.Current osteoporosis reports · 2023Review
- Lineage-specific differences and regulatory networks governing human chondrocyte development.eLife · 2023Article
- Emerging RUNX2-Mediated Gene Regulatory Mechanisms Consisting of Multi-Layered Regulatory Networks in Skeletal Development.International journal of molecular sciences · 2023Review
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- Single-cell chromatin accessibility profiling of cell-state-specific gene regulatory programs during mouse organogenesis.Frontiers in neuroscience · 2023Article
- Stat5a promotesAmerican journal of translational research · 2023Article
- A mineralizing pool of Gli1-expressing progenitors builds the tendon enthesis and demonstrates therapeutic potential.Cell stem cell · 2022Article
- Runx2 regulates chromatin accessibility to direct the osteoblast program at neonatal stages.Cell reports · 2022Article
- The developmental impacts of natural selection on human pelvic morphology.Science advances · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
During endochondral ossification, small, immature chondrocytes enlarge to form hypertrophic chondrocytes, which express collagen X. In this work, we demonstrate that FoxA factors are induced during chondrogenesis, bind to conserved binding sites in the collagen X enhancer, and can promote the expression of a collagen X-luciferase reporter in both chondrocytes and fibroblasts. In addition, we demonstrate by both gain- and loss-of-function analyses that FoxA factors play a crucial role in driving the expression of both endogenous collagen X and other hypertrophic chondrocyte-specific genes. Mice engineered to lack expression of both FoxA2 and FoxA3 in their chondrocytes display defects in chondrocyte hypertrophy, alkaline phosphatase expression, and mineralization in their sternebrae and, in addition, exhibit postnatal dwarfism that is coupled to significantly decreased expression of both collagen X and MMP13 in their growth plates. Our findings indicate that FoxA family members are crucial regulators of the hypertrophic chondrocyte differentiation program.
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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.