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<p>Intervertebral disc degeneration (IDD) is the main cause of low back pain and is related to the aging of nucleus pulposus (NP) cells (NPCs). However, the underlying mechanism for senescence of NPCs has not been well understood. NPCs (control-NPCs and IDD-NPCs) were separated from the NP tissues of patients, diagnosed with graded I and IV IDD. The proliferation and senescence levels were detected by MTT assay and senescence-associated β-galactosidase staining, respectively. The expression of cyclin B1 and caveolin-1 was evaluated by Western blot analysis. RNA-sequencing technology was used to screen differentially expressed genes (DEGs) in IDD-NPCs. Finally, through the interference and overexpression of MYB proto-oncogene-like 2 (MYBL2), the effect of MYBL2 on cell senescence was explored. Compared with control-NPCs, the proliferation ability of IDD-NPCs was significantly reduced and the senescence level was obviously increased. 1,061 DEGs were screened in IDD-NPCs. By analyzing DEGs related to aging and aging-related pathways and terms, cell cycle arrest was identified. Knockdown of MYBL2 promoted the senescence of control-NPCs, and overexpression of MYBL2 inhibited the senescence of IDD-NPCs. The study found that upregulation of MYBL2 ameliorated the senescence of IDD-NPCs, providing a potential way to inhibit the senescence of NPCs.</p>

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Upregulation of MYBL2 ameliorates senescence of nucleus pulposus cells in degenerative intervertebral discs based on RNA-sequencing analysis

  • 期刊论文

  • 发表日期：

    2026年1月7日

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  • Shenghui Tang,
  • Tao Liu,
  • Lixue Wu,
  • Ximing Xu,
  • Le Huan,
  • Xiaofei Sun,
  • Yuan Wang

摘要

Intervertebral disc degeneration (IDD) is the main cause of low back pain and is related to the aging of nucleus pulposus (NP) cells (NPCs). However, the underlying mechanism for senescence of NPCs has not been well understood. NPCs (control-NPCs and IDD-NPCs) were separated from the NP tissues of patients, diagnosed with graded I and IV IDD. The proliferation and senescence levels were detected by MTT assay and senescence-associated β-galactosidase staining, respectively. The expression of cyclin B1 and caveolin-1 was evaluated by Western blot analysis. RNA-sequencing technology was used to screen differentially expressed genes (DEGs) in IDD-NPCs. Finally, through the interference and overexpression of MYB proto-oncogene-like 2 (MYBL2), the effect of MYBL2 on cell senescence was explored. Compared with control-NPCs, the proliferation ability of IDD-NPCs was significantly reduced and the senescence level was obviously increased. 1,061 DEGs were screened in IDD-NPCs. By analyzing DEGs related to aging and aging-related pathways and terms, cell cycle arrest was identified. Knockdown of MYBL2 promoted the senescence of control-NPCs, and overexpression of MYBL2 inhibited the senescence of IDD-NPCs. The study found that upregulation of MYBL2 ameliorated the senescence of IDD-NPCs, providing a potential way to inhibit the senescence of NPCs.