Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Small RNA sequencing reveals miR-204 as a miRNA potentially associated with OA development.
  • Fig. S2. Validation of p16INK4a detection and its up-regulation in OA and aged mouse cartilage.
  • Fig. S3. Effect of H2O2 long-term treatment on the cell viability of mouse chondrocytes.
  • Fig. S4. Validation of cellular senescence in chondrocytes by IR.
  • Fig. S5. Validation of cellular senescence in chondrocytes after bleomycin or doxorubicin treatment.
  • Fig. S6. miR-204 expression in chondrocytes is not regulated by the senescence-associated cell cycle arrest regulators, p53 and p16INK4a.
  • Fig. S7. miR-204 expression in chondrocytes is regulated by GATA4 and NF-κB.
  • Fig. S8. Intra-articular injection of miR-204 does not elicit synovial inflammation but induces MMP13 expression in articular cartilage.
  • Fig. S9. Transcriptome-wide coexpression analysis reveals that miR-204 inactivates putative functional modules related to PG synthesis, cell cycle, or programmed cell death.
  • Fig. S10. miR-204 targets multiple genes involved in PG biosynthesis pathways in mouse primary chondrocytes and human chondrosarcoma cells.
  • Fig. S11. Negative controls for immunohistochemistry.
  • Fig. S12. Quantification of CS to measure the effect of miR-204 on PG accumulation in mouse articular cartilage.
  • Fig. S13. Effect of miR-204 on SOX9 and aggrecan expression in primary cultured mouse chondrocytes and knee joint cartilage.
  • Fig. S14. Knockdown efficiency of siRNAs designed for miR-204 target genes.
  • Fig. S15. miR-204 decreases the chain length and sulfation extent of CS chains in PGs.
  • Fig. S16. miR-204 antagonism does not affect SA-β-Gal activity but suppresses the SASP factors Timp2 and Igfbp7 in chondrocytes.
  • Fig. S17. miR-204 antagonism suppresses the expression of Adamts5 and Il1b in senescent chondrocytes.
  • Fig. S18. miR-204 inhibition by anti–miR-204 does not affect the appearance of articular cartilage in sham-operated mice but suppresses p16INK4a expression in articular cartilage of DMM-operated mice.
  • Fig. S19. Schematic representation of the senescence-induced signaling pathway mediated by miR-204 in OA development.
  • Fig. S20. Uncropped gel images with size markers from the indicated figures.
  • Table S1. Descriptive characteristics of human patients with OA.
  • Table S2. List of siRNAs, miRNAs, and anti-miR.
  • Table S3. List of PCR primers.
  • Table S4. List of PCR primers for cloning.
  • References (85–97)

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