ArticleDevelopment (Cambridge, England)2016
Retinoic acid-induced premature osteoblast-to-preosteocyte transitioning has multiple effects on calvarial development.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 31 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 drives cell fate specification, maturation and retinal regionality in human retinal organoids.Nature communications · 2026Article
- SPP1 is a plasma biomarker associated with the dia gnosis and prediction of prognosis in sepsis.Scientific reports · 2024Article
- Insights into Craniofacial Development and Anomalies: Exploring Fgf Signaling in Zebrafish Models.Current osteoporosis reports · 2024Review
- Article
- Role of vitamins beyond vitamin DInternational journal of molecular medicine · 2024Review
- Vitamin C protects retinal ganglion cells via SPP1 in glaucoma and after optic nerve damage.Life science alliance · 2023Article
- Direct BMP signaling to chordoblasts is required for the initiation of segmented notochord sheath mineralization in zebrafish vertebral column development.Frontiers in endocrinology · 2023Article
- The endocannabinoid system and retinoic acid signaling combine to influence bone growth.Molecular and cellular endocrinology · 2021Article
- Pharmacological Manipulation of Early Zebrafish Skeletal Development Shows an Important Role for Smad9 in Control of Skeletal Progenitor Populations.Biomolecules · 2021Article
- Rare functional genetic variants in COL7A1, COL6A5, COL1A2 and COL5A2 frequently occur in Chiari Malformation Type 1.PloS one · 2021Article
- Regulating Retinoic Acid Availability during Development and Regeneration: The Role of the CYP26 Enzymes.Journal of developmental biology · 2020Review
- New Insights into the Control of Cell Fate Choices and Differentiation by Retinoic Acid in Cranial, Axial and Caudal Structures.Biomolecules · 2019Review
- Article
- Osteocytogenesis: Roles of Physicochemical Factors, Collagen Cleavage, and Exogenous Molecules.Tissue engineering. Part B, Reviews · 2018Review
- Direct activation of chordoblasts by retinoic acid is required for segmented centra mineralization during zebrafish spine development.Development (Cambridge, England) · 2018Article
- Genetic advances in craniosynostosis.American journal of medical genetics. Part A · 2017Review
- Article
- Building and maintaining joints by exquisite local control of cell fate.Wiley interdisciplinary reviews. Developmental biology · 2017Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously shown that, in human and zebrafish, hypomorphic mutations of the gene encoding the retinoic acid (RA)-metabolizing enzyme Cyp26b1 result in coronal craniosynostosis, caused by an RA-induced premature transitioning of suture osteoblasts to preosteocytes, inducing ectopic mineralization of the suture's osteoid matrix. In addition, we showed that human CYP26B1 null patients have more severe and seemingly opposite skull defects, characterized by smaller and fragmented calvaria, but the cellular basis of these defects remained largely unclear. Here, by treating juvenile zebrafish with exogenous RA or a chemical Cyp26 inhibitor in the presence or absence of osteogenic cells or bone-resorbing osteoclasts, we demonstrate that both reduced calvarial size and calvarial fragmentation are also caused by RA-induced premature osteoblast-to-preosteocyte transitioning. During calvarial growth, the resulting osteoblast deprival leads to decreased osteoid production and thereby smaller and thinner calvaria, whereas calvarial fragmentation is caused by increased osteoclast stimulation through the gained preosteocytes. Together, our data demonstrate that RA-induced osteoblast-to-preosteocyte transitioning has multiple effects on developing bone in Cyp26b1 mutants, ranging from gain to loss of bone, depending on the allelic strength, the developmental stage and the cellular context.
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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.