ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2013
Suppression of autophagy by FIP200 deletion leads to osteopenia in mice through the inhibition of osteoblast terminal differentiation.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.
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127 citing papers in PubMed, 222 citations in OpenAlex.
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- Inflammaging-Driven Osteoporosis: Is a Galectin-Targeted Approach Needed?International journal of molecular sciences · 2025Review
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- CYB5A promotes osteogenic differentiation of MC3T3-E1 cells through autophagy mediated by the AKT/mTOR/ULK1 signaling pathway.Scientific reports · 2025Article
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- Pharmacological mechanism of natural products to treat osteoporosis: a focus on the autophagy.Frontiers in pharmacology · 2025Review
- SEC31a-ATG9a Interaction Mediates the Recruitment of COPII Vesicles for Autophagosome Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Autophagy, a double-edged sword for oral tissue regeneration.Journal of advanced research · 2024Review
- AMPK activation enhances osteoblast differentiation on a titanium disc via autophagy.International journal of implant dentistry · 2024Article
67 more citing papers are in PubMed but not listed here.
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9 authors at 1 institution in 1 country.
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Abstract
Autophagy is a conserved lysosomal degradation process that has important roles in both normal human physiology and disease. However, the function of autophagy in bone homeostasis is not well understood. Here, we report that autophagy is activated during osteoblast differentiation. Ablation of focal adhesion kinase family interacting protein of 200 kD (FIP200), an essential component of mammalian autophagy, led to multiple autophagic defects in osteoblasts including aberrantly increased p62 expression, deficient LC3-II conversion, defective autophagy flux, absence of GFP-LC3 puncta in FIP200-null osteoblasts expressing transgenic GFP-LC3, and absence of autophagosome-like structures by electron microscope examination. Osteoblast-specific deletion of FIP200 led to osteopenia in mice. Histomorphometric analysis revealed that the osteopenia was the result of cell-autonomous effects of FIP200 deletion on osteoblasts. FIP200 deletion led to defective osteoblast terminal differentiation in both primary bone marrow and calvarial osteoblasts in vitro. Interestingly, both proliferation and differentiation were not adversely affected by FIP200 deletion in early cultures. However, FIP200 deletion led to defective osteoblast nodule formation after initial proliferation and differentiation. Furthermore, treatment with autophagy inhibitors recapitulated the effects of FIP200 deletion on osteoblast differentiation. Taken together, these data identify FIP200 as an important regulator of bone development and reveal a novel role of autophagy in osteoblast function through its positive role in supporting osteoblast nodule formation and differentiation.
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