Skip to main content
. 2021 Jan 29;12(1):141–157. doi: 10.1016/j.jcmgh.2021.01.016

Figure 7.

Figure 7

CD73-generated extracellular adenosine activates AMPK in hepatocytes and livers from CD73-LKO mice and show impaired AMPK signaling. (A) Representative immunoblots of AMPK substrate phosphorylation in liver lysates from male and female mice. (B) Semiquantitative analysis of AMPK substrate phosphorylation relative to total protein based on immunoblots in panel A. ∗∗∗P < .0001, 2-way analysis of variance. Error bars represent SD. (C) Fresh-frozen liver sections were stained with antibodies against AMPK (red) and zonula occludens 1 (ZO1) (green) show similar AMPK distribution in WT and CD73-LKO mice. Bottom panels: Magnified view of the boxed areas. Scale bar: 50 μm. (D) Isolated WT hepatocytes were treated with AMP and recombinant soluble CD73 (rCD73) at the indicated concentrations. Representative immunoblots of total and phospho-AMPKα. (E) Quantification of phosphorylated/total AMPK. n = 4 replicates. ∗∗P < .001; 2-way analysis of variance. (F) Representative immunoblot analysis showing AMPK phosphorylation in WT hepatocytes treated with AMP, rCD73, and the adenosine transport inhibitor nitrobenzylthioinosine (NBTI). (G) Quantification of phosphorylated/total AMPK in rCD73-treated hepatocytes, in the absence/presence of AMP and NBTI. n = 3 replicates. 2-way analysis of variance. Error bars represent SD. DAPI, 4′,6-diamidino-2-phenylindole.