MiR-21 modulates P.g-LPS induced apoptosis and inflammatory response in HUVECs via NF-κB/iNOS/NO pathway by targeting PDCD4

作者：Jing Ren, Huiqiong Zou, Siyu Sun, Shan Chen, Rui He, Qianbing Zhou, Jun Tao, Junying Yang · 发表于：Non-coding RNA Research · 年份：2025 · DOI：10.1016/j.ncrna.2025.10.001 · 被引用次数：2 · 研究领域：MicroRNA in disease regulation、Cancer-related molecular mechanisms research、NF-κB Signaling Pathways

Porphyromonas gingivalis lipopolysaccharide ( P.g- LPS), a key virulence factor in periodontitis, contributes to systemic vascular diseases, notably atherosclerosis. MicroRNA-21 (miR-21), a critical post-transcriptional regulator, influences inflammation and vascular pathology, but its role in endothelial responses to P.g- LPS remains unclear. Gingival biopsies from eight patients with periodontitis and eight healthy controls were analyzed using immunofluorescence co-labeling for Cluster of Differentiation 31(CD31) with TUNEL or Interleukin-6 (IL-6) to assess endothelial apoptosis and inflammation. MiR-21 levels were quantified using quantitative Reverse Transcription Polymerase Chain Reaction(RT-PCR). Human umbilical vein endothelial cells (HUVECs) were treated with P.g- LPS and transfected with miR-21 mimics or inhibitors. Apoptosis, proliferation, and migration were evaluated by flow cytometry, Cell Counting Kit-8(CCK-8) assay, and wound healing analysis, respectively. Western blotting and Enzyme-Linked Immunosorbent Assay(ELISA) measured inflammatory and apoptotic markers. Luciferase reporter assays confirmed that PDCD4 was a direct target of miR-21, and the effects of Programmed Cell Death 4(PDCD4) knockdown on Nuclear Factor kappa B(NF-κB)/Inducible Nitric Oxide Synthase(iNOS)/Nitric Oxide(NO) signaling were examined. Endothelial cells from patients with periodontitis exhibited increased apoptosis and inflammation. P.g- LPS significantly reduced miR-21 expression in HUV...