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. 2017 Jul 7;7:4880. doi: 10.1038/s41598-017-05033-5

Figure 6.

Figure 6

Activation of NLRP3 in myeloid cells causes excessive production of IL-1β, a cytokine that promotes chondrocyte death. (A) Bone marrow cells were centrifuged at 400 × g, and the supernatants were harvested for IL-1β measurement. **P < 0.005. (B) Western blot analysis of the effects of IL-1β on PARP1 cleavage in chondrocytes. Cells were treated with IL-1β for 24 hours. β-actin was used as loading control. Cont, control. qPCR analysis of the expression of HIF-1α (C), VEGF (D), Ca9 (E), PGK1 (F), Glut1 (G) and Binp3 (H). RNA were isolated from murine chondrocytes from the ribs of 2-day old pups. Data are expressed as the mean ± SEM. *P < 0.05; **P < 0.005; Cont, control. Rel, relative. NS, not significant. ELISA analysis of IL-1β levels in conditioned media (I) and Western blot analysis of NLRP3 expression (J) from BMM treated with 100 ng/ml LPS for 3 hours, then with 5 mM ATP for 30 minutes in normoxic or hypoxic conditions. Data are representative of 2–3 independent experiments and expressed as mean ± SEM. *P < 0.05; **P < 0.005; $P < 0.001 vs. WT normoxia + LPS.