Loss of AMP-Activated Protein Kinase Induces Mitochondrial Dysfunction and Proinflammatory Response in Unstimulated Abcd1-Knockout Mice Mixed Glial Cells

Figure 1

Adenosine monophosphate activated protein kinase (AMPKα1) levels are similar in vivo in wild type (WT) and Abcd1-knockout (KO) central nervous systems and in vitro in mixed glial cells. (a) Age-matched (3-month-old) WT and Abcd1-KO mice were sacrificed and the brains and spinal cords harvested for AMPKα1 protein (i) and mRNA (ii) levels. (b) In primary mixed glial cells from WT and Abcd1-KO mice, AMPKα1 protein (i) and mRNA (ii) levels were similar. (b) Abcd1-KO mixed glial cells were silenced for scrambled control (Scr) or AMPKα1 as described in Section 2. Lentiviral vector silencing with AMPKα1-shRNA significantly decreased the AMPKα1 protein (i) and mRNA (ii) levels in Abcd1-KO mice primary mixed glial cells. Results represent the mean ± SD of triplicates from three different experiments. AMPKα1 silenced compared with scrambled (Scr) silenced.

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