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. 2021 Jan;29(1):89–99. doi: 10.1016/j.joca.2020.08.002

Fig. 4.

Fig. 4

TRPV4 activation abolishes IL-1β inflammatory signalling via HDAC6 activation. Levels of (A) nitrite (B) PGE2 and (C) COX-2 expression associated with isolated chondrocytes ± IL-1β (1 ng/ml) in the presence or absence of GSK101 for 24 h. GSK101 promotes (D) HDAC6 activity, induces the (E) de-acetylation and (E) de-polymerization of α-tubulin, as measured by Western blot of acetylated α-tubulin (Acet α-Tub), α-tubulin (α-Tub) and non-polymerized α-tubulin. Full western blots can be found in supplementary figure S9 (G) HDAC6 inhibition with tubacin (500 nM) abolished the anti-inflammatory effect of GSK101 on NO release. Data represents mean ± SD for n = 6 (A, B, D and G) and n = 4 (C, E and F) Statistics: Two-way ANOVA and post hoc Tukey's test (A–C), T-test (D-G. # represents statistically significant difference between IL-1β treated and corresponding untreated cells.