Figure 5: AMPKα deficiency enhancing phospho-NF-κB p65 and the procatabolic response to iterleukin-1β (IL-1β) in primary murine chondrocytes. | Scientific Reports

Figure 5: AMPKα deficiency enhancing phospho-NF-κB p65 and the procatabolic response to iterleukin-1β (IL-1β) in primary murine chondrocytes.

From: AMPK deficiency in chondrocytes accelerated the progression of instability-induced and ageing-associated osteoarthritis in adult mice

Figure 5

Primary articular chondrocytes were isolated from Col2a1-CreERT2; AMPKα1flox/floxα2flox/flox mice and their Cre-negative WT littermates and treated with 4-hydroxytamoxifen for 48 hours as described in the Methods. (a) Western blotting analyses of AMPKα expression. (b) The expression levels of Col2a1, Aggrecan, Sox9, MMP-3, MMP-13, Adamts4, Adamts5 and Timp3 messenger RNA (mRNA) in primary murine chondrocytes treated with or without IL-1β (10 ng/ml) for 24 h were determined by real-time reverse transcriptase-PCR. Data are representative of three individual experiments. Col2a1 = Type II collagen; MMP-3 = matrix metalloproteinase-3; MMP-13 = matrix metalloproteinase-13; *p < 0.05. ***p < 0.001. NS = not significant. (c) Western blotting analyses of total NF-κB p65 and phospho-NF-κB p65 in primary murine chondrocytes with or without IL-1β (10 ng/ml) for 24 h. Increased phospho-NF-κB p65 protein expression in chondrocytes from AMPKα cDKO mice compared with their WT littermates was observed. GAPDH served as a loading control.

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