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GOLGB1 deficiency accelerates intervertebral disc degeneration by activating the MAPK pathway
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  • Published: 17 January 2026

GOLGB1 deficiency accelerates intervertebral disc degeneration by activating the MAPK pathway

  • Jingyuan Tian1,2,3 na1,
  • Zhiquan Wang3,4 na1,
  • Ruxing Liu2,3,
  • Xiaoting Qiu2,3,
  • Dongqin He2,3,
  • Nan Shan2,3,
  • Qichao Li2,3,
  • Guanghui He2,3,
  • Bin Zhao2,3,
  • Jie Yuan2,3 &
  • …
  • Yongfeng Wang2,3 

Scientific Reports , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Apoptosis
  • Chronic inflammation

Abstract

Intervertebral disc degeneration (IDD) is a multifactorially regulated age-related condition. Golgin B1 (GOLGB1) is a large Golgi-related transmembrane protein encoded by golgb1 gene. Since its discovery, GOLGB1 has been proved to be related to many diseases. However, its role in IDD is still unclear. The aim of this research was to examine whether GOLGB1 deficiency accelerates disc degeneration and to study its mechanism. We selected C57BL/6 male mice aged 8 weeks to isolate, culture and identify nucleus pulposus (NP) cells, and used a variety of experimental techniques, including plasmid transfection, western blotting (WB), real-time fluorescence quantitative PCR (RT-qPCR), EdU staining, Tunnel staining, CCK8 and flow cytometry (FCM) to detect the effects of GOLGB1 on the degeneration, proliferation and apoptosis of NP cells in vitro. Then, 8-week-old C57BL/6 male mice were selected for caudal vertebra acupuncture to establish IDD model, and the role and mechanism of GOLGB1 in the development of IDD were studied by HE staining, Safranin O-Fast Green staining, Alcian Blue staining and immunohistochemistry (IHC) staining. Our results demonstrated lower expression of GOLGB1 in human tissues with NP degeneration. Additionally, GOLGB1 expression was reduced in NP tissue from aging adult mice and IDD model mice. We further verified that GOLGB1 knockdown worsened NP cell degeneration, disturbed the composition of the extracellular matrix (ECM), and upset the harmony between anabolism and catabolism. Moreover, GOLGB1 knockdown inhibited the proliferation of NP cells and increased the apoptosis of NP cells. Mechanistically, GOLGB1 knockdown elevated p-ERK and p-P38 levels and activated the MAPK pathway. A MAPK signaling pathway inhibitor (SCH772984) strongly reversed this phenomenon and rescued the degeneration of NP cells. These findings suggest that GOLGB1 may be a potential new target for IDD. GOLGB1 is a protective factor against disc degeneration, and knockdown of GOLGB1 accelerates IDD by activating the MAPK pathway.

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Data availability

The data used to support the findings of this study will be available with the request to the corresponding author.

Abbreviations

IDD:

Intervertebral disc degeneration

GOLGB1:

Golgin B1

NP:

Nucleus pulposus

WB:

Western blotting

RT-qPCR:

Real-time fluorescence quantitative PCR

FCM:

Flow cytometry

IHC:

Immunohistochemistry

ECM:

Extracellular matrix

LBP:

Low back pain

BSA:

Bovine serum albumin

FBS:

Fetal bovine serum

EdU:

5-Ethynyl-2'-deoxyuridine

CCK8:

Cell counting kit-8

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Acknowledgements

We thank the Shanxi key Laboratory of Bone and Soft Tissue Injury Repair of the Second Hospital of Shanxi Medical University for its experimental environment and equipment support.

Funding

Shanxi Province Higher Education “Billion Project” Science and Technology Guidance Project (BYJL030 and BYJL013); the Natural Science Foundation of Shanxi Province, China (202203021211040 and 20210302124670); Shanxi Provincial Science and Technology Cooperation and Exchange Special Project (202104041101023).

Author information

Author notes
  1. Jingyuan Tian and Zhiquan Wang Contributed equaly to this work.

Authors and Affiliations

  1. Department of Orthopedics, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China

    Jingyuan Tian

  2. Department of Shanxi key Laboratory of Bone and Soft Tissue Injury Repair, Second Hospital of Shanxi Medical University, Taiyuan, 030001, China

    Jingyuan Tian, Ruxing Liu, Xiaoting Qiu, Dongqin He, Nan Shan, Qichao Li, Guanghui He, Bin Zhao, Jie Yuan & Yongfeng Wang

  3. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shanxi Medical University, Taiyuan, 030001, China

    Jingyuan Tian, Zhiquan Wang, Ruxing Liu, Xiaoting Qiu, Dongqin He, Nan Shan, Qichao Li, Guanghui He, Bin Zhao, Jie Yuan & Yongfeng Wang

  4. The People’s Hospital of Linfen, Linfen, 041000, China

    Zhiquan Wang

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Contributions

All authors contributed to the study conception and design. The study was designed by Y.-F. W., B. Z., and J. Y. The data collections were performed by J.-Y. T., Z.-Q. W., R.X. L., X.T. Q. and D.Q. H. The statistical analyses were performed by J.Y. T., N. S. and G.-H. H. The data interpretations were performed by Z.-Q. W. and Q.C. L. The literature searches were performed by all authors. The funds collection was provided by J. Y. and Y.-F. W. Finally, the first draft of the manuscript was written by J.-Y. T. and Z.-Q. W., and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Bin Zhao, Jie Yuan or Yongfeng Wang.

Ethics declarations

Competing interests

The authors declare no competing interests.

Ethics approval and consent to participate

This study was approved by the Ethics Committee of the Second Hospital of Shanxi Medical University (approval number: 2021YX Number 019) and written informed consent was acquired from all participants. Animal procedures involving C57BL/6 mice were strictly authorized by the Ethics Committee of the Animal Transformation Center of Shanxi Medical University (approval number: DW2022053), which complies with the Guide for the Care and Use of Laboratory Animals, published by the United States National Institutes of Health (2011). All methods in the present study were designed and performed in accordance with ARRIVE guidelines and the other relevant guidelines and regulations.

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Tian, J., Wang, Z., Liu, R. et al. GOLGB1 deficiency accelerates intervertebral disc degeneration by activating the MAPK pathway. Sci Rep (2026). https://doi.org/10.1038/s41598-025-34797-4

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  • Received: 19 September 2024

  • Accepted: 31 December 2025

  • Published: 17 January 2026

  • DOI: https://doi.org/10.1038/s41598-025-34797-4

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Keywords

  • GOLGB1
  • Intervertebral disc degeneration
  • MAPK pathway
  • Proliferation
  • Apoptosis
  • Extracellular matrix
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