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<p>To explore the role and mechanism of long non-coding RNA SLC7A11-AS1 in lipopolysaccharide-induced injury of human periodontal ligament stem cells (hPDLSCs) via regulation of microRNA-1260 (miR-1260), and to assess its diagnostic value in periodontitis. Serum levels of SLC7A11-AS1 and miR-1260 were measured by qRT-PCR in 80 periodontitis patients and 80 healthy controls. Diagnostic performance was evaluated using receiver operating characteristic (ROC) analysis and correlation with periodontal indices. hPDLSCs were treated with 2&#xa0;µg/mL LPS to induce inflammation; SLC7A11-AS1 was silenced by siRNA and miR-1260 inhibited by inhibitor. Cell viability, apoptosis, expression of Cyclin D1, Bcl-2, and Bax, inflammatory cytokines, and oxidative stress markers were assessed. Direct interaction was confirmed by dual-luciferase reporter assay. Serum SLC7A11-AS1 was up-regulated in periodontitis (<i>P</i> &lt; 0.001) with high diagnostic accuracy (AUC = 0.8047) and positive correlation with PLI, SBI, PD, and AL (r = 0.716–0.740, <i>P</i> &lt; 0.001). miR-1260 was down-regulated and inversely correlated with SLC7A11-AS1 (r = –0.713, <i>P</i> &lt; 0.001). In hPDLSCs, LPS induced SLC7A11-AS1 expression, reduced viability, increased apoptosis, and altered Cyclin D1, Bcl-2, and Bax levels; these effects were reversed by SLC7A11-AS1 knockdown and reinstated by miR-1260 inhibition. SLC7A11-AS1 sponged miR-1260, modulating inflammatory and oxidative responses. SLC7A11-AS1 exacerbates LPS-induced hPDLSC injury by negatively regulating miR-1260, representing a potential biomarker and therapeutic target in periodontitis.</p>

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LncRNA SLC7A11-AS1 is involved in human periodontal stem cell injury by negatively regulating miR-1260 expression

  • 期刊论文

  • 发表日期：

    2025年8月25日

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  • Junyi Zheng,
  • Pingying Zhang,
  • Huimin Xie,
  • Zhengyi Chu,
  • Baohua Xu

摘要

To explore the role and mechanism of long non-coding RNA SLC7A11-AS1 in lipopolysaccharide-induced injury of human periodontal ligament stem cells (hPDLSCs) via regulation of microRNA-1260 (miR-1260), and to assess its diagnostic value in periodontitis. Serum levels of SLC7A11-AS1 and miR-1260 were measured by qRT-PCR in 80 periodontitis patients and 80 healthy controls. Diagnostic performance was evaluated using receiver operating characteristic (ROC) analysis and correlation with periodontal indices. hPDLSCs were treated with 2 µg/mL LPS to induce inflammation; SLC7A11-AS1 was silenced by siRNA and miR-1260 inhibited by inhibitor. Cell viability, apoptosis, expression of Cyclin D1, Bcl-2, and Bax, inflammatory cytokines, and oxidative stress markers were assessed. Direct interaction was confirmed by dual-luciferase reporter assay. Serum SLC7A11-AS1 was up-regulated in periodontitis (P < 0.001) with high diagnostic accuracy (AUC = 0.8047) and positive correlation with PLI, SBI, PD, and AL (r = 0.716–0.740, P < 0.001). miR-1260 was down-regulated and inversely correlated with SLC7A11-AS1 (r = –0.713, P < 0.001). In hPDLSCs, LPS induced SLC7A11-AS1 expression, reduced viability, increased apoptosis, and altered Cyclin D1, Bcl-2, and Bax levels; these effects were reversed by SLC7A11-AS1 knockdown and reinstated by miR-1260 inhibition. SLC7A11-AS1 sponged miR-1260, modulating inflammatory and oxidative responses. SLC7A11-AS1 exacerbates LPS-induced hPDLSC injury by negatively regulating miR-1260, representing a potential biomarker and therapeutic target in periodontitis.