Supplementary Materials

The PDF file includes:

• Materials and Methods
• Fig. S1. Early postnatal Prx1-mediated ablation of Tgfbr2 generates long-term TGFBR2 deficits in joint cell populations.
• Fig. S2. In mice with TGFBR2-deficient joint cell populations, evidence of abnormal cartilage morphology appears within days of Tgfbr2 ablation and persists through early postnatal development.
• Fig. S3. Postnatal ablation of Tgfbr2 leads to an OA-like cartilage phenotype at P3M and P6M.
• Fig. S4. Postnatal ablation of Tgfbr2 leads to a severe OA-like phenotype in multiple joint tissues that is concomitant with up-regulation of MMP13 at P14M.
• Fig. S5. Postnatal ablation of Tgfbr2 in Tgfbr2^−/− mutants leads to accelerated posttraumatic OA.
• Fig. S6. Postnatal ablation of Tgfbr2 leads to up-regulation of IL-36α and IL-36Ra at P14M.
• Fig. S7. DMM surgery induces an expression change of TGFBR2 in synovium region interfacing with the articular cartilage.
• Fig. S8. DMM surgeries induce expression changes of TGFBR2, IL-36α, IL-36r, and IL-36Ra in articular cartilage.
• Fig. S9. Low dose of i.a. injection of IL-36Ra and IL-36α has no effect on the articular phenotype of Tgfbr2^−/− mice.
• Fig. S10. Analysis of IL-36α, IL-36R, IL-36RN, MMP13, and TGFBR2 in histological and end-stage OA.
• Fig. S11. Histologically prepared sections of end-stage OA cartilage specimens.
• Fig. S12. mRNA expression of Sox9, collagen 2, aggrecan, Adamts4, Adamts5, and Mmp3 in histological and end-stage OA.
• Fig. S13. Human chondrocytes treated with IL-36α exhibit a dose-dependent activation of MAPK and NF-κB signaling pathways.
• Fig. S14. RT-PCR results of Sox9, collagen 2, aggrecan, Adamts4, Adamts5, and Mmp3 in IL-36α-treated human articular chondrocytes.
• References (56–61)

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Other Supplementary Material for this manuscript includes the following:

• Data file S1 (Microsoft Excel format). Primary data.