CircTTC3 regulates the osteogenic differentiation of adipose-derived mesenchymal stem cells via miR-205/Smad3 axis.
Zhang Q., Guo Z., Hu W., Tang W., Gao X., Han C.
Animal Study, published in Exp Cell Res (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Exp Cell Res (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40915343
- DOI
- 10.1016/j.yexcr.2025.114746
Abstract (original English)
Adipose-derived mesenchymal stem cells (ADSCs) hold great promise for bone tissue repair and regeneration. Circular RNAs (circRNAs) play a crucial role in regulating the osteogenic differentiation and bone remodeling of ADSCs; however, the underlying molecular mechanisms remain unclear. In this study, we conducted whole transcriptome sequencing (WTS) on ADSCs and constructed a competing endogenous RNA (ceRNA) regulatory network to identify the circTTC3/miR-205/mothers against decapentaplegic homolog 3 (Smad3) signaling axis. Subsequently, we used Sanger sequencing and agarose gel electrophoresis to verify the cyclization of circTTC3. We confirmed that circTTC3 promotes the osteogenic differentiation of ADSCs and demonstrated that circTTC3 co-localizes with miR-205 in the cytoplasm. Additionally, we showed that circTTC3 sponges miR-205 using dual-luciferase reporter assays and fluorescent in situ hybridization (FISH) experiments. Moreover, miR-205 targets the 3' untranslated region (UTR) of Smad3. Rescue experiments further verified that circTTC3 mediates the osteogenic differentiation of ADSCs through the miR-205/Smad3 pathway. Finally, in vivo, animal studies revealed that circTTC3 overexpression enhances cranial defect repair while silencing circTTC3 disrupts new bone formation.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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