ArticleJournal of orthopaedic surgery and research2024
ZFP36, an RNA-binding protein promotes hBMSCs osteogenic differentiation via binding with JUN.
Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- RNA-binding proteins in aging and age-related diseases: roles, mechanisms, and a large language model analysis.Biogerontology · 2026Review
- The acid-sensing ion channel 1a modulates anxiety- and depression-related behaviors via its influencing on the activity of corticotropin-releasing hormone-expressing neurons in the hypothalamic paraventricular nucleus in male mice.Translational psychiatry · 2026Article
- Integrative Single-Cell RNA Sequencing and Machine Learning Reveals Candidate Plasma Protein-Associated Gene Signatures for Osteoporosis: A Preliminary Exploratory in Silico Study.International journal of general medicine · 2026Article
- Single-Cell Transcriptomic Analysis Suggests That JUN May Regulate BAMBI to Promote Osteosarcoma Cell Migration and Invasion.Human mutation · 2026Article
- Hyperoside promotes osteoblast differentiation by increasing osteoclast-derived migrasomes to alleviate osteoporosis.American journal of translational research · 2026Article
- Identification of palmitoylated biomarkers in non-alcoholic fatty liver disease via integrated bioinformatics analysis and machine learning.Scientific reports · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Osteoporosis (OP) is a metabolic bone disease characterized by progressive decline of bone mass and bone quality, leading to bone fragility and an increased risk of fracture. The osteogenic differentiation of bone mesenchymal stem cells (BMSCs) is crucial to maintain the balance of osteoblast and osteoclast. Bioinformatics prediction indicates that ZFP36 ring finger protein (ZFP36), an RNA-binding protein, is a potential target of OP. Herein, we sought to probe the regulatory role and mechanisms of ZFP36 in the progression of OP. Overexpression of ZFP36 enhanced osteoblast viability, differentiation and mineralization of human BMSCs (hBMSCs). RNA immunoprecipitation qPCR (RIP-qPCR) assays demonstrated that ZFP36 could inhibit the translation of JUN, which was also verified with dual luciferase reporter gene assay. Furthermore, administration with T-5224, a transcription factor c-Fos/activator protein (AP)-1 inhibitor, which specifically inhibits the DNA binding activity of c-Fos/JUN, abolished the effect of ZFP36 knockdown on the behaviors of hBMSCs, suggesting that ZFP36 might promotes osteogenic differentiation through regulating JUN. These findings provide insights into the progression and a potential therapeutic target of OP.
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Registered trials
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