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<p>Keloids are a fibroproliferative skin disorder. Exploring the mechanism of keloid formation is crucial for advancing treatment efficacy. Here, we investigated the mechanism of extracellular vesicles (EVs) derived from human adipose-derived mesenchymal stem cells (ADSCs) on the abnormal proliferation of human keloid fibroblasts (KFs) through delivering miR-182-5p, aiming to explore the underlying molecular mechanism. ADSCs were isolated and identified via morphological observation, osteogenic/adipogenic differentiation assays, and flow cytometry for surface marker analysis. ADSC-EVs were isolated by ultracentrifugation and characterized using TEM, NTA, and Western blot. KFs and normal fibroblasts were collected. EV internalization was confirmed by PKH26 labeling, and EV-dependent delivery of miR-182-5p was verified via FAM-labeled miRNA and RNase A/Triton X100 treatment. Cell proliferation was evaluated. Binding of miR-182-5p to ZNF217 was predicted by RNA22 and validated via dual-luciferase reporter assays. ZNF217 overexpression was performed to confirm the role of the miR-182-5p/ZNF217 axis. ADSC-EVs significantly inhibited KF proliferation. miR-182-5p carried by ADSC-EVs suppressed ZNF217 expression. ZNF217 overexpression reversed the inhibitory effect of miR-182-5p overexpression in ADSC-EVs on KF proliferation. In conclusion, ADSC-EVs inhibit KF proliferation via the miR-182-5p/ZNF217 axis, thereby interfering with the early stage of scar formation. This study provides a novel target for cell-free therapy of keloids.</p>

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Molecular mechanisms of miR-182-5p carried by adipose-derived mesenchymal stem cell extracellular vesicles in human fibroblasts proliferation

  • 期刊论文

  • 发表日期：

    2026年7月23日

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  • Xiaoye Yuan,
  • Yong Song

摘要

Keloids are a fibroproliferative skin disorder. Exploring the mechanism of keloid formation is crucial for advancing treatment efficacy. Here, we investigated the mechanism of extracellular vesicles (EVs) derived from human adipose-derived mesenchymal stem cells (ADSCs) on the abnormal proliferation of human keloid fibroblasts (KFs) through delivering miR-182-5p, aiming to explore the underlying molecular mechanism. ADSCs were isolated and identified via morphological observation, osteogenic/adipogenic differentiation assays, and flow cytometry for surface marker analysis. ADSC-EVs were isolated by ultracentrifugation and characterized using TEM, NTA, and Western blot. KFs and normal fibroblasts were collected. EV internalization was confirmed by PKH26 labeling, and EV-dependent delivery of miR-182-5p was verified via FAM-labeled miRNA and RNase A/Triton X100 treatment. Cell proliferation was evaluated. Binding of miR-182-5p to ZNF217 was predicted by RNA22 and validated via dual-luciferase reporter assays. ZNF217 overexpression was performed to confirm the role of the miR-182-5p/ZNF217 axis. ADSC-EVs significantly inhibited KF proliferation. miR-182-5p carried by ADSC-EVs suppressed ZNF217 expression. ZNF217 overexpression reversed the inhibitory effect of miR-182-5p overexpression in ADSC-EVs on KF proliferation. In conclusion, ADSC-EVs inhibit KF proliferation via the miR-182-5p/ZNF217 axis, thereby interfering with the early stage of scar formation. This study provides a novel target for cell-free therapy of keloids.