Bioinformatic prediction of key genes involved in pro-chondrogenic effect of fragmentated cartilage transplantation

TL;DR

This study finds that minced cartilage fragments improve cartilage repair more than chunk fragments, possibly due to inflammation-related gene activity.

Contribution

The study identifies differentially expressed genes linked to cartilage repair efficacy and suggests inflammation's role in pro-chondrogenic effects.

Findings

Minced cartilage fragments improved cartilage repair outcomes compared to chunk fragments and fibrin glue alone.

RNA-seq analysis identified 75 differentially expressed genes, with up-regulated genes linked to inflammation and cell proliferation.

Down-regulated genes in minced fragments showed a negative relationship with cell migration and inflammation.

Abstract

Minced cartilage transplantation is thought to promote cartilage repair. However, the underlying mechanisms remain less well understood. In this study, we established a rat osteochondral defect model to evaluate fragment size-dependent repair efficacy, and tried to explore the mechanisms preliminarily. Herein, rats with cartilage defect were randomly divided into 3 groups. Small allogeneic cartilage fragments with fibrin glue, chunk allogeneic cartilage fragments with fibrin glue, and only fibrin glue were used to treat cartilage defects in each group, respectively. The results showed that the minced cartilage fragments had significantly improved outcomes in promoting cartilage repairing compared to chunk cartilage fragments and only fibrin glue. Notably, particulated cartilage transplantation-treat cartilage lesion had elevated inflammation. Following RNA-seq analysis on cartilage fragments and cartilage chunk identified 75 differentially expressed genes (DEGs), which include 70 up-regulated DEGs and 5 down-regulated DEGs in cartilage fragment group (CFG). Further GO enrichment and KEGG pathway analysis showed that the up-regulated DEGs in CFG were mainly involved in inflammation, cell proliferation and migration. We also found that the down-regulated DEGs in CFG had negative relationship with cell migration, proliferation and inflammation. This study suggest that cartilage fragmentation enhances repair efficacy compared to chunk cartilage transplantation, and the mechanism of pro-chondrogenic effect may be related to inflammatory stimulation.

The online version contains supplementary material available at 10.1038/s41598-025-05961-7.

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