ArticleExperimental & molecular medicine2015
Caveolin-1 regulates osteoclast differentiation by suppressing cFms degradation.
Article in Experimental & molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
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- The genomic response of human granulosa cells (KGN) to melatonin and specific agonists/antagonists to the melatonin receptors.Scientific reports · 2022Article
- RANKL/RANK promotes the migration of gastric cancer cells by interacting with EGFR.Clinical and translational medicine · 2020Article
- ST5 Positively Regulates Osteoclastogenesis via Src/Syk/calcium Signaling Pathways.Molecules and cells · 2019Article
- SMPDL3b modulates insulin receptor signaling in diabetic kidney disease.Nature communications · 2019Article
- Anti-neoplastic drugs increase caveolin-1-dependent migration, invasion and metastasis of cancer cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caveolae are flask-shaped cell-surface membranes, which consist of cholesterol, sphingolipids and caveolin proteins. In a microarray analysis, we found that caveolin-1 (Cav-1) was upregulated by receptor activator of NFκB ligand (RANKL), the osteoclast differentiation factor. Silencing of Cav-1 inhibited osteoclastogenesis and also decreased the activation of mitogen-activated protein kinase and the induction of NFATc1 by RANKL. Cav-1 knockdown suppressed the expression of cFms and RANK, two major receptors for osteoclastogenesis. Interestingly, cFms expression was decreased only at the protein level, not at the messenger RNA (mRNA) level, whereas RANK expression was decreased at both the mRNA and protein levels. Furthermore, Cav-1 deficiency increased the lysosomal degradation of cFms. Taken together, these results demonstrate that Cav-1-dependent cFms stabilization contributes to efficient osteoclastogenesis.
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