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Background <p>Peroxiredogenase 2 (PRDX2) has been confirmed to be downregulated in patients with intervertebral disc degeneration (IDD). However, the role and mechanism of PRDX2 in the progression of IDD are still unclear.</p> Methods <p>Tert-butyl hydroperoxide (TBHP)-induced nucleus pulposus (NP) cells were used to construct IDD conditions. qRT-PCR or western blot was used to detect the expression levels of PRDX2, ubiquitin-specific protease 11 (USP11), ferroptosis-related markers and extracellular matrix (ECM)-related proteins. CCK8 assay, TUNEL assay and detection of ferroptosis-related markers were performed to examine cell viability, apoptosis and ferroptosis. Co-IP assay and ubiquitination assay were used to explore the regulation of USP11 on PRDX2.</p> Results <p>The expression levels of PRDX2 and USP11 were reduced in IDD patients and TBHP-induced NP cells. PRDX2 overexpression repressed TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation. Moreover, our study found that USP11 stabilized the protein expression of PRDX2 by decreasing its ubiquitination. In addition, USP11 overexpression inhibited TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation, while these effects were reversed by PRDX2 knockdown.</p> Conclusion <p>USP11-mediated deubiquitination of PRDX2 might alleviate IDD progression by inhibiting TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation, providing a potential intervention target worthy of further research for IDD.</p>

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Ubiquitination-mediated PRDX2 alleviates intervertebral disc degeneration via restraining TBHP-induced nucleus pulposus cell apoptosis, ferroptosis and ECM degradation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月24日

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  • Fanguo Kong,
  • Jiyao Luan,
  • Qipeng Pan,
  • Yang Qiao,
  • Wenju Wang

摘要

Background

Peroxiredogenase 2 (PRDX2) has been confirmed to be downregulated in patients with intervertebral disc degeneration (IDD). However, the role and mechanism of PRDX2 in the progression of IDD are still unclear.

Methods

Tert-butyl hydroperoxide (TBHP)-induced nucleus pulposus (NP) cells were used to construct IDD conditions. qRT-PCR or western blot was used to detect the expression levels of PRDX2, ubiquitin-specific protease 11 (USP11), ferroptosis-related markers and extracellular matrix (ECM)-related proteins. CCK8 assay, TUNEL assay and detection of ferroptosis-related markers were performed to examine cell viability, apoptosis and ferroptosis. Co-IP assay and ubiquitination assay were used to explore the regulation of USP11 on PRDX2.

Results

The expression levels of PRDX2 and USP11 were reduced in IDD patients and TBHP-induced NP cells. PRDX2 overexpression repressed TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation. Moreover, our study found that USP11 stabilized the protein expression of PRDX2 by decreasing its ubiquitination. In addition, USP11 overexpression inhibited TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation, while these effects were reversed by PRDX2 knockdown.

Conclusion

USP11-mediated deubiquitination of PRDX2 might alleviate IDD progression by inhibiting TBHP-induced NP cell apoptosis, ferroptosis and ECM degradation, providing a potential intervention target worthy of further research for IDD.