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Background <p>The aim of this study is to investigate whether LINC00673 and leptin are associated with osteogenesis of periodontal ligament stem cells in the microenvironment of advanced glycation end products.</p> Methods <p>LINC00673 expression was detected in PDLSCs by qRT-PCR performed during osteogenic differentiation. By using alkaline phosphatase and Alizarin red S staining, we were able to confirm the role of LINC00673 in regulating osteogenesis in PDLSCs. Assays were performed on nude mice to test bone regeneration in the dorsal region to investigate MiR-188-3p’s binding to LINC00673 and leptin (LEP). Western blot was used to detect osteoblast markers (COL1, ALP and RUNX2).</p> Results <p>As predicted, miR-188-3p interacts with LINC00673 directly, and miR-188-3p overexpression increases osteogenic differentiation. However, overexpression of LINC00673 reversed this effect, suggesting that LINC00673 functions as a competing endogenous RNA for miR-188-3p. A regulatory network formed by LINC00673 and miR-188-3p regulates the expression of LEP, a gene that inhibits the canonical Wnt pathway, reducing bone formation in PDLSCs.</p> Conclusions <p>PDLSCs differentiate osteogenically as a result of a regulatory network between lncRNA and miRNA (microRNA), which may serve as a therapeutic target for diabetes-related periodontitis.</p>

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LINC00673 binds with leptin to regulate osteogenic function in periodontal ligament stem cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月14日

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  • Yang Yang,
  • Peng Yang,
  • Yuxing Zhang,
  • Zhaoyan Wu,
  • Xuxia Wang,
  • Jun Zhang

摘要

Background

The aim of this study is to investigate whether LINC00673 and leptin are associated with osteogenesis of periodontal ligament stem cells in the microenvironment of advanced glycation end products.

Methods

LINC00673 expression was detected in PDLSCs by qRT-PCR performed during osteogenic differentiation. By using alkaline phosphatase and Alizarin red S staining, we were able to confirm the role of LINC00673 in regulating osteogenesis in PDLSCs. Assays were performed on nude mice to test bone regeneration in the dorsal region to investigate MiR-188-3p’s binding to LINC00673 and leptin (LEP). Western blot was used to detect osteoblast markers (COL1, ALP and RUNX2).

Results

As predicted, miR-188-3p interacts with LINC00673 directly, and miR-188-3p overexpression increases osteogenic differentiation. However, overexpression of LINC00673 reversed this effect, suggesting that LINC00673 functions as a competing endogenous RNA for miR-188-3p. A regulatory network formed by LINC00673 and miR-188-3p regulates the expression of LEP, a gene that inhibits the canonical Wnt pathway, reducing bone formation in PDLSCs.

Conclusions

PDLSCs differentiate osteogenically as a result of a regulatory network between lncRNA and miRNA (microRNA), which may serve as a therapeutic target for diabetes-related periodontitis.