Scholarlink

<p>The persistence of wounds can cause limitations in the normal movement of patients. This study investigated the effects of long noncoding RNA (lncRNA) SNHG1 and miR-199a-3p on wound healing. In vitro skin wound modelling using LPS-induced keratinocytes. SNHG1 and miR-199a-3p levels were assessed by RT-qPCR. CCK-8 was used to determine the cells proliferative. Cell migration was analyzed using Transwell. Cell apoptosis was detected using flow cytometry. The inflammatory factors levels by ELISA assay. DLR assay was used to validate the binding of SNHG1 to miR-199a-3p targets. Increased SNHG1 levels, decreased proliferation and migration, and increased apoptosis in successfully modelled cells. Inflammatory factors levels were notably increased in the treated cells. The cells proliferative and migratory were restored, the apoptosis rate decreased and inflammatory factors levels decreased after SNHG1 knockdown. Molecularly, SNHG1 targets miR-199a-3p. The increase in cell proliferation and migration caused by SNHG1 knockdown was reversed by the addition of miR-199a-3p inhibitor. Apoptosis rate was increased, as were the levels of inflammatory factors. Silencing SNHG1 induced miR-199a-3p high expression, which contributed to the proliferative and migratory activities of HaCaT cells, promoting the shift of cells from the inflammatory phase to the proliferative phase and facilitating wound healing.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

LncRNA SNHG1 regulates human keratinocyte function by targeting miR-199a-3p to delay skin wound healing

  • 期刊论文

  • 发表日期：

    2025年3月29日

查看全文
  • Xuejuan Zan,
  • Bin Liu,
  • Huajiang Liu,
  • Ting Yu,
  • Yu Cao

摘要

The persistence of wounds can cause limitations in the normal movement of patients. This study investigated the effects of long noncoding RNA (lncRNA) SNHG1 and miR-199a-3p on wound healing. In vitro skin wound modelling using LPS-induced keratinocytes. SNHG1 and miR-199a-3p levels were assessed by RT-qPCR. CCK-8 was used to determine the cells proliferative. Cell migration was analyzed using Transwell. Cell apoptosis was detected using flow cytometry. The inflammatory factors levels by ELISA assay. DLR assay was used to validate the binding of SNHG1 to miR-199a-3p targets. Increased SNHG1 levels, decreased proliferation and migration, and increased apoptosis in successfully modelled cells. Inflammatory factors levels were notably increased in the treated cells. The cells proliferative and migratory were restored, the apoptosis rate decreased and inflammatory factors levels decreased after SNHG1 knockdown. Molecularly, SNHG1 targets miR-199a-3p. The increase in cell proliferation and migration caused by SNHG1 knockdown was reversed by the addition of miR-199a-3p inhibitor. Apoptosis rate was increased, as were the levels of inflammatory factors. Silencing SNHG1 induced miR-199a-3p high expression, which contributed to the proliferative and migratory activities of HaCaT cells, promoting the shift of cells from the inflammatory phase to the proliferative phase and facilitating wound healing.