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<p><i>Staphylococcus aureus</i>-induced bone infection is one of the thorny issues in clinical orthopedics, and understanding its detailed molecular regulatory mechanisms will help in seeking strategies. In this study, the differentially expressed genes in murine long bone osteocyte (MLO)-Y4 cells treated with or without <i>Staphylococcus aureus</i> were screened out through RNA sequencing, and microtubule actin crosslinking factor 1 (MACF1) was identified as one of the most significantly downregulated genes, which was validated by the subsequent RT-qPCR and Western blot. Then, Cellular functional assays showed that MACF1 overexpression markedly inhibited apoptosis and secretion of inflammatory mediators, but recovered cell viability and production of osteogenic markers in staphylococcal protein A (SPA) induced MLO-Y4 cells. Mechanistically, MACF1 mRNA was stabilized by N6 methyl adenosine (m6A) modification, and upregulated MACF1 inactivated the PI3K/AKT signaling in SPA-induced MLO-Y4 cells. To conclude, targeting m6A-methylated MACF1 ameliorates SPA-triggered inflammation, apoptosis and metabolic dysfunction in MLO-Y4 cells.</p>

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N6 methyl adenosine-stabilized microtubule actin crosslinking factor 1 ameliorates staphylococcal protein A-induced damage in osteocyte-like MLO-Y4 cells

  • 期刊论文

  • 发表日期：

    2026年7月28日

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  • Siyu Lu,
  • Muguo Song,
  • Lirong Ren,
  • Junyi Li,
  • Kehan Lv,
  • Jian Shi,
  • Yongqing Xu

摘要

Staphylococcus aureus-induced bone infection is one of the thorny issues in clinical orthopedics, and understanding its detailed molecular regulatory mechanisms will help in seeking strategies. In this study, the differentially expressed genes in murine long bone osteocyte (MLO)-Y4 cells treated with or without Staphylococcus aureus were screened out through RNA sequencing, and microtubule actin crosslinking factor 1 (MACF1) was identified as one of the most significantly downregulated genes, which was validated by the subsequent RT-qPCR and Western blot. Then, Cellular functional assays showed that MACF1 overexpression markedly inhibited apoptosis and secretion of inflammatory mediators, but recovered cell viability and production of osteogenic markers in staphylococcal protein A (SPA) induced MLO-Y4 cells. Mechanistically, MACF1 mRNA was stabilized by N6 methyl adenosine (m6A) modification, and upregulated MACF1 inactivated the PI3K/AKT signaling in SPA-induced MLO-Y4 cells. To conclude, targeting m6A-methylated MACF1 ameliorates SPA-triggered inflammation, apoptosis and metabolic dysfunction in MLO-Y4 cells.