ArticlePloS one2015
Deletion of IFT80 Impairs Epiphyseal and Articular Cartilage Formation Due to Disruption of Chondrocyte Differentiation.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 53 citations in OpenAlex.
- Disruption of distal appendage protein CEP164 causes skeletal malformation in mice.Biochemical and biophysical research communications · 2024Article
- A loss of primary cilia by a reduction in mTOR signaling correlates with age-related deteriorations in condylar cartilage.GeroScience · 2024Article
- Skeletal ciliopathy: pathogenesis and related signaling pathways.Molecular and cellular biochemistry · 2024Review
- Orbital shaking conditions augment human nasoseptal cartilage formation in 3D culture.Frontiers in bioengineering and biotechnology · 2024Article
- Mechanotransduction pathways in articular chondrocytes and the emerging role of estrogen receptor-α.Bone research · 2023Review
- From mesenchymal niches to engineeredMaterials today. Bio · 2022Article
- Type II collagen-positive progenitors are important stem cells in controlling skeletal development and vascular formation.Bone research · 2022Article
- Primary Cilia Direct Murine Articular Cartilage Tidemark Patterning Through Hedgehog Signaling and Ambulatory Load.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Ciliary IFT88 Protects Coordinated Adolescent Growth Plate Ossification From Disruptive Physiological Mechanical Forces.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Article
- Primary Cilia: A Cellular Regulator of Articular Cartilage Degeneration.Stem cells international · 2022Review
- Role of Primary Cilia in Skeletal Disorders.Stem cells international · 2022Review
- SAG therapy restores bone growth and reduces enchondroma incidence in a model of skeletal chondrodysplasias caused by Ihh deficiency.Molecular therapy. Methods & clinical development · 2021Article
- Type II collagen-positive embryonic progenitors are the major contributors to spine and intervertebral disc development and repair.Stem cells translational medicine · 2021Article
- Ttc30a affects tubulin modifications in a model for ciliary chondrodysplasia with polycystic kidney disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Wdpcp regulates cellular proliferation and differentiation in the developing limb via hedgehog signaling.BMC developmental biology · 2021Article
- Low-Dose Tamoxifen Induces Significant Bone Formation in Mice.JBMR plus · 2021Article
- The Primary Cilium on Cells of Developing Skeletal Rudiments; Distribution, Characteristics and Response to Mechanical Stimulation.Frontiers in cell and developmental biology · 2021Article
- Ciliary IFT80 is essential for intervertebral disc development and maintenance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Mechanotransduction pathways in the regulation of cartilage chondrocyte homoeostasis.Journal of cellular and molecular medicine · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Intraflagellar transport proteins (IFT) play important roles in cilia formation and organ development. Partial loss of IFT80 function leads Jeune asphyxiating thoracic dystrophy (JATD) or short-rib polydactyly (SRP) syndrome type III, displaying narrow thoracic cavity and multiple cartilage anomalies. However, it is unknown how IFT80 regulates cartilage formation. To define the role and mechanism of IFT80 in chondrocyte function and cartilage formation, we generated a Col2α1; IFT80f/f mouse model by crossing IFT80f/f mice with inducible Col2α1-CreER mice, and deleted IFT80 in chondrocyte lineage by injection of tamoxifen into the mice in embryonic or postnatal stage. Loss of IFT80 in the embryonic stage resulted in short limbs at birth. Histological studies showed that IFT80-deficient mice have shortened cartilage with marked changes in cellular morphology and organization in the resting, proliferative, pre-hypertrophic, and hypertrophic zones. Moreover, deletion of IFT80 in the postnatal stage led to mouse stunted growth with shortened growth plate but thickened articular cartilage. Defects of ciliogenesis were found in the cartilage of IFT80-deficient mice and primary IFT80-deficient chondrocytes. Further study showed that chondrogenic differentiation was significantly inhibited in IFT80-deficient mice due to reduced hedgehog (Hh) signaling and increased Wnt signaling activities. These findings demonstrate that loss of IFT80 blocks chondrocyte differentiation by disruption of ciliogenesis and alteration of Hh and Wnt signaling transduction, which in turn alters epiphyseal and articular cartilage formation.
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Registered trials
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