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<p>Hypertrophic scar (HS) represents an excessive fibrotic response during the healing of skin injuries, constituting a common and intricate pathological process that is tightly regulated. This study aimed to explore the clinical significance and potential mechanisms of long non-coding RNA CRNDE in the development of HS. This study encompassed 71 HS patients, and the expression levels of lncRNA CRNDE were assessed via RT-qPCR. Concurrently, the concentrations of collagen I A1 and collagen III A1 were quantified using the Enzyme-linked immunosorbent assay (ELISA) technique, while the cellular activities of hypertrophic scar fibroblasts (HSFs) were evaluated through CCK-8 assays, Transwell migration assays, and flow cytometry. Furthermore, a dual-luciferase reporter gene assay was conducted to confirm the target interaction between CRNDE and microRNA -29a-3p. LncRNA CRNDE was markedly upregulated in HS tissues. Silencing lncRNA CRNDE led to a reduction in collagen I A1 and collagen III A1 levels in HSFs, inhibited cell proliferation and migration, and simultaneously promoted cell apoptosis. Moreover, miR-29a-3p expression was downregulated in HS tissues and exhibited a negative correlation with lncRNA CRNDE expression. The effects of lncRNA CRNDE knockdown on collagen I A1/ III A1 levels, cell proliferation, migration, and apoptosis could be partially mitigated by a miR-29a-3p inhibitor. LncRNA CRNDE influenced the biological behaviors of HS through its interaction with miR-29a-3p.</p>

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Long non-coding RNA CRNDE promotes the progress of hypertrophic scar via regulating the proliferation and migration of hypertrophic scar fibroblasts through targeting microRNA-29a-3p

  • 期刊论文

  • 发表日期：

    2025年2月20日

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  • Zhaohua Wang,
  • Xiaohua Wu,
  • Li Zeng

摘要

Hypertrophic scar (HS) represents an excessive fibrotic response during the healing of skin injuries, constituting a common and intricate pathological process that is tightly regulated. This study aimed to explore the clinical significance and potential mechanisms of long non-coding RNA CRNDE in the development of HS. This study encompassed 71 HS patients, and the expression levels of lncRNA CRNDE were assessed via RT-qPCR. Concurrently, the concentrations of collagen I A1 and collagen III A1 were quantified using the Enzyme-linked immunosorbent assay (ELISA) technique, while the cellular activities of hypertrophic scar fibroblasts (HSFs) were evaluated through CCK-8 assays, Transwell migration assays, and flow cytometry. Furthermore, a dual-luciferase reporter gene assay was conducted to confirm the target interaction between CRNDE and microRNA -29a-3p. LncRNA CRNDE was markedly upregulated in HS tissues. Silencing lncRNA CRNDE led to a reduction in collagen I A1 and collagen III A1 levels in HSFs, inhibited cell proliferation and migration, and simultaneously promoted cell apoptosis. Moreover, miR-29a-3p expression was downregulated in HS tissues and exhibited a negative correlation with lncRNA CRNDE expression. The effects of lncRNA CRNDE knockdown on collagen I A1/ III A1 levels, cell proliferation, migration, and apoptosis could be partially mitigated by a miR-29a-3p inhibitor. LncRNA CRNDE influenced the biological behaviors of HS through its interaction with miR-29a-3p.