ArticlePloS one2019
Atoh8 acts as a regulator of chondrocyte proliferation and differentiation in endochondral bones.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Integrative analysis of the 3D genome and epigenome in mouse embryonic tissues.Nature structural & molecular biology · 2025Article
- Thyroid hormone induces ossification and terminal maturation in a preserved OA cartilage biomimetic model.Arthritis research & therapy · 2024Article
- ATOH8 Expression Is Regulated by BMP2 and Plays a Key Role in Human Endometrial Stromal Cell Decidualization.Endocrinology · 2023Article
- Article
- The temporal transcriptomic signature of cartilage formation.Nucleic acids research · 2023Article
- Lineage-specific differences and regulatory networks governing human chondrocyte development.eLife · 2023Article
- Agonists of prostaglandin EProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Atoh8 in Development and Disease.Biology · 2022Review
- Atonal homolog 8/Math6 regulates differentiation and maintenance of skeletal muscle.Frontiers in cell and developmental biology · 2022Article
- Long non-coding RNA CIR inhibits chondrogenic differentiation of mesenchymal stem cells by epigenetically suppressing ATOH8 via methyltransferase EZH2.Molecular medicine (Cambridge, Mass.) · 2021Article
- BMP-induced Atoh8 attenuates osteoclastogenesis by suppressing Runx2 transcriptional activity and reducing the Rankl/Opg expression ratio in osteoblasts.Bone research · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atonal homolog 8 (Atoh8) is a transcription factor of the basic helix-loop-helix (bHLH) protein family, which is expressed in the cartilaginous elements of endochondral bones. To analyze its function during chondrogenesis we deleted Atoh8 in mice using a chondrocyte- (Atoh8flox/flox;Col2a1-Cre) and a germline- (Atoh8flox/flox;Prx1-Crefemale) specific Cre allele. In both strains, Atoh8 deletion leads to a reduced skeletal size of the axial and appendicular bones, but the stages of phenotypic manifestations differ. While we observed obviously shortened bones in Atoh8flox/flox;Col2a1-Cre mice only postnatally, the bones of Atoh8flox/flox;Prx1-Crefemale mice are characterized by a reduced bone length already at prenatal stages. Detailed histological and molecular investigations revealed reduced zones of proliferating and hypertrophic chondrocytes. In addition, Atoh8 deletion identified Atoh8 as a positive regulator of chondrocyte proliferation. As increased Atoh8 expression is found in the region of prehypertrophic chondrocytes where the expression of Ihh, a main regulator of chondrocyte proliferation and differentiation, is induced, we investigated a potential interaction of Atoh8 function and Ihh signaling. By activating Ihh signaling with Purmorphamine we demonstrate that Atoh8 regulates chondrocyte proliferation in parallel or downstream of Ihh signaling while it acts on the onset of hypertrophy upstream of Ihh likely by modulating Ihh expression levels.
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Registered trials
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