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<p>This study aims to investigate the role and underlying mechanism of the long non-coding RNA (lncRNA) LOC100912399 in regulating osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), with a specific focus on its involvement in oxidative stress-induced apoptosis via the p38 mitogen-activated protein kinase (p38MAPK) signaling pathway. BMSCs were isolated from the tibiae and fibulae of Sprague-Dawley (SD) rat pups and cultured to the third passage. Cell purity was confirmed by flow cytometric analysis of surface markers (CD45, CD29, CD106, CD90, CD11b), and multilineage differentiation potential was verified using Alizarin Red S (osteogenic), Oil Red O (adipogenic), and Alcian Blue (chondrogenic) staining. At 90% confluence, BMSCs were transduced with lentiviral vectors for LOC100912399 overexpression (Lv-LOC100912399) or knockdown (Sh-LOC100912399), alone or in combination with p38MAPK pathway inhibition or overexpression (Lv-p38MAPK), followed by exposure to oxidative stress for 48&#xa0;h. Apoptosis was evaluated by Annexin V/PI staining, cell viability by CCK-8 assay, and gene expression by quantitative real-time PCR (qRT-PCR). Protein levels of oxidative stress-related enzymes (MnSOD, CAT, GPx), apoptosis-related factors (Bcl-2, Bax, p-p38MAPK), and osteogenic markers (RUNX2, OPN, ALP) were determined by Western blot. High-purity BMSCs (&gt; 99%) were successfully isolated and characterized. Overexpression of LOC100912399 significantly promoted oxidative stress-induced apoptosis, reduced cell viability, downregulated antioxidant enzyme expression, increased the Bax/Bcl-2 ratio, and inhibited osteogenic differentiation (<i>P</i> &lt; 0.05). Conversely, knockdown of LOC100912399 enhanced antioxidant capacity, suppressed apoptosis, and upregulated osteogenic marker expression (<i>P</i> &lt; 0.05). These effects were further modulated by either p38MAPK overexpression or inhibition, indicating that LOC100912399 functions, at least in part, through the p38MAPK signaling pathway. LOC100912399 regulates oxidative stress and apoptosis in BMSCs via the p38MAPK signaling pathway, thereby influencing osteogenic differentiation. Targeting LOC100912399 may represent a potential therapeutic strategy for enhancing bone formation under oxidative stress-related conditions such as osteoporosis.</p>

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LOC100912399 regulates osteogenic differentiation of bone marrow mesenchymal stem cells through modulating p38MAPK signaling-mediated oxidative stress and apoptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月1日

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  • Cheng-Song Lan,
  • Pao Wang,
  • Teng Kang,
  • Hao Qin,
  • Zhi-Wei Liu,
  • Sheng-Jie Gu,
  • Jing-Peng Zhang,
  • Gang Liu

摘要

This study aims to investigate the role and underlying mechanism of the long non-coding RNA (lncRNA) LOC100912399 in regulating osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), with a specific focus on its involvement in oxidative stress-induced apoptosis via the p38 mitogen-activated protein kinase (p38MAPK) signaling pathway. BMSCs were isolated from the tibiae and fibulae of Sprague-Dawley (SD) rat pups and cultured to the third passage. Cell purity was confirmed by flow cytometric analysis of surface markers (CD45, CD29, CD106, CD90, CD11b), and multilineage differentiation potential was verified using Alizarin Red S (osteogenic), Oil Red O (adipogenic), and Alcian Blue (chondrogenic) staining. At 90% confluence, BMSCs were transduced with lentiviral vectors for LOC100912399 overexpression (Lv-LOC100912399) or knockdown (Sh-LOC100912399), alone or in combination with p38MAPK pathway inhibition or overexpression (Lv-p38MAPK), followed by exposure to oxidative stress for 48 h. Apoptosis was evaluated by Annexin V/PI staining, cell viability by CCK-8 assay, and gene expression by quantitative real-time PCR (qRT-PCR). Protein levels of oxidative stress-related enzymes (MnSOD, CAT, GPx), apoptosis-related factors (Bcl-2, Bax, p-p38MAPK), and osteogenic markers (RUNX2, OPN, ALP) were determined by Western blot. High-purity BMSCs (> 99%) were successfully isolated and characterized. Overexpression of LOC100912399 significantly promoted oxidative stress-induced apoptosis, reduced cell viability, downregulated antioxidant enzyme expression, increased the Bax/Bcl-2 ratio, and inhibited osteogenic differentiation (P < 0.05). Conversely, knockdown of LOC100912399 enhanced antioxidant capacity, suppressed apoptosis, and upregulated osteogenic marker expression (P < 0.05). These effects were further modulated by either p38MAPK overexpression or inhibition, indicating that LOC100912399 functions, at least in part, through the p38MAPK signaling pathway. LOC100912399 regulates oxidative stress and apoptosis in BMSCs via the p38MAPK signaling pathway, thereby influencing osteogenic differentiation. Targeting LOC100912399 may represent a potential therapeutic strategy for enhancing bone formation under oxidative stress-related conditions such as osteoporosis.