ArticleMolecular and cellular biology2013
ADAM17 controls endochondral ossification by regulating terminal differentiation of chondrocytes.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- ADAM17 and its proteolytic targets in disease pathogenesis.The FEBS journal · 2026Review
- Structural basis for ADAM17 activation by the iRhom1 pseudoprotease.Cell reports · 2026Article
- Structural insights into the activation and inhibition of the ADAM17-iRhom2 complex.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Downregulation of the metalloproteinases ADAM10 or ADAM17 promotes osteoclast differentiation.Cell communication and signaling : CCS · 2024Article
- Article
- Analysis of the function of ADAM17 in iRhom2 curly-bare and tylosis with esophageal cancer mutant mice.Journal of cell science · 2023Article
- Epidermal growth factor signalling pathway in endochondral ossification: an evidence-based narrative review.Annals of medicine · 2022Review
- Identification of Molecular Determinants in iRhoms1 and 2 That Contribute to the Substrate Selectivity of Stimulated ADAM17.International journal of molecular sciences · 2022Article
- Heat Shock Alters the Proteomic Profile of Equine Mesenchymal Stem Cells.International journal of molecular sciences · 2022Article
- Regulation of osteoarthritis development by ADAM17/Tace in articular cartilage.Journal of bone and mineral metabolism · 2022Article
- Strategies to Target ADAM17 in Disease: From its Discovery to the iRhom Revolution.Molecules (Basel, Switzerland) · 2021Review
- Role of iRhoms 1 and 2 in Endochondral Ossification.International journal of molecular sciences · 2020Article
- Alteration of the Total Cellular Glycome during Late Differentiation of Chondrocytes.International journal of molecular sciences · 2019Article
- IL-6 exhibits bothThe Journal of biological chemistry · 2019Article
- EGFR Signaling: Friend or Foe for Cartilage?JBMR plus · 2019Review
- Roles for HB-EGF in Mesenchymal Stromal Cell Proliferation and Differentiation During Skeletal Growth.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- A New Look at Causal Factors of Idiopathic Scoliosis: Altered Expression of Genes Controlling Chondroitin Sulfate Sulfation and Corresponding Changes in Protein Synthesis in Vertebral Body Growth Plates.International journal of medical sciences · 2019Article
- Expression of the ectodomain-releasing protease ADAM17 is directly regulated by the osteosarcoma and bone-related transcription factor RUNX2.Journal of cellular biochemistry · 2018Article
- Intriguing Roles for Endothelial ADAM10/Notch Signaling in the Development of Organ-Specific Vascular Beds.Physiological reviews · 2018Review
- Elf3 Contributes to Cartilage Degradation in vivo in a Surgical Model of Post-Traumatic Osteoarthritis.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Endochondral ossification is a highly regulated process that relies on properly orchestrated cell-cell interactions in the developing growth plate. This study is focused on understanding the role of a crucial regulator of cell-cell interactions, the membrane-anchored metalloproteinase ADAM17, in endochondral ossification. ADAM17 releases growth factors, cytokines, and other membrane proteins from cells and is essential for epidermal growth factor receptor (EGFR) signaling and for processing tumor necrosis factor alpha. Here, we report that mice lacking ADAM17 in chondrocytes (A17ΔCh) have a significantly expanded zone of hypertrophic chondrocytes in the growth plate and retarded growth of long bones. This abnormality is caused by an accumulation of the most terminally differentiated type of chondrocytes that produces a calcified matrix. Inactivation of ADAM17 in osteoclasts or endothelial cells does not affect the zone of hypertrophic chondrocytes, suggesting that the main role of ADAM17 in the growth plate is in chondrocytes. This notion is further supported by in vitro experiments showing enhanced hypertrophic differentiation of primary chondrocytes lacking Adam17. The enlarged zone of hypertrophic chondrocytes in A17ΔCh mice resembles that described in mice with mutant EGFR signaling or lack of its ligand transforming growth factor α (TGFα), suggesting that ADAM17 regulates terminal differentiation of chondrocytes during endochondral ossification by activating the TGFα/EGFR signaling axis.
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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.