miR-10955-5p Targets ITPKB to Regulate Proliferation and Differentiation in Thiram-Induced Tibial Dyschondroplasia Chondrocytes
Tibial dyschondroplasia (TD) is a common skeletal disorder in fast-growing broiler chickens that compromises leg health and production efficiency. However, the post-transcriptional mechanisms underlying TD remain poorly understood. Based on previous sequencing data showing that miR-10955-5p was downregulated in TD cartilage, this study investigated its role in TD chondrocyte proliferation and differentiation through in vitro functional assays. Quantitative real-time PCR (RT-qPCR), CCK-8, EdU, flow cytometry, bioinformatic prediction, dual-luciferase reporter assays, and rescue experiments were performed. Overexpression of miR-10955-5p promoted chondrocyte proliferation and differentiation and reduced apoptosis, whereas inhibition of miR-10955-5p produced the opposite effects. Inositol-trisphosphate 3-kinase B (ITPKB) was identified as a direct target of miR-10955-5p. ITPKB overexpression suppressed chondrocyte proliferation and differentiation, while co-overexpression of miR-10955-5p partially reversed these inhibitory effects. These findings indicate that miR-10955-5p positively regulates chondrocyte proliferation and viability, at least in part, by repressing ITPKB expression. The miR-10955-5p-ITPKB axis provides new insight into the molecular regulation of chondrocyte dysfunction in TD and may serve as a potential molecular target for further investigation.
Authors
- Xinqi Wang (ORCID: https://orcid.org/0000-0002-4589-4912)
- Shiyu Yang (ORCID: https://orcid.org/0000-0002-6222-0389)
- Yan Wang (ORCID: https://orcid.org/0000-0002-3477-1458)
- Hengyong Xu
- Xu-yang Ji (ORCID: https://orcid.org/0009-0002-4458-2180)
- Ting Yang
- Long-Ge Guo
- Zhi Hu
Institutions
- Sichuan Agricultural University (CN)
- Ministry of Agriculture and Rural Affairs (CN)
Publication Details
- Journal
- Life
- Published
- 2026-10-27
- DOI
- https://doi.org/10.3390/life16111809
- Primary Topic
- Osteoarthritis Treatment and Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00