ArticleCell and tissue banking2022
Co-culture with Sirt1-overexpressed chondrocytes delays the nucleus pulposus cells degeneration.
Article in Cell and tissue banking, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- Cell-based therapies for intervertebral disc degeneration: Navigating the path from promise to clinical reality.Journal of orthopaedic translation · 2026Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Nucleus pulposus cells (NPCs) degeneration is an essential pathological basis of intervertebral disc diseases, and autologous cell transplantation is a means of regeneration of NPCs. This study aimed to evaluate the effects of autologous facet joint chondrocytes (CHs) with Sirtuin 1 (sirt1)-overexpression on NPCs degeneration. We used human NPCs and CHs isolated from the patients' tissue and transduced CHs with the plasmid vector to overexpress the sirt1 gene. Further, NPCs were seeded as monolayers and treated with IL-1β to obtain the degeneration, and the sirt1-overexpressed CHs (sirt1-CHs) in the transwell insert were co-cultured in the same well. The NPCs' degenerated degree was determined by the levels of living cells, proliferation, p16, and collagen I/II, and aggrecan expression at the time point of 1, 3, or 5 days. Besides, the ROS accumulation, antioxidative enzymes, sirt1, and inflammatory factors gene expression were also tested. After IL-1β treatment, when co-cultured with sirt1-CHs, NPCs accumulated more living cells, proliferation, collagen II, aggrecan, but less p16 and collagen I expression than cultured without sirt1-CHs. Additionally, SOD1, CAT, and TIMP4 mRNA were protected, and the production of TNF-α, IL-6, MMP3, and ROS were alleviated with the presence of sirt1-CHs. Thus, co-culture with sirt1-CHs delays NPCs' degeneration via the suppression of ROS accumulation and inflammatory response. Transplanting autologous CHs with sirt1-overexpressed into the NP tissue might be a novel treatment for intervertebral disc degeneration.
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