Fig. 7.
Iron loading changes the balance between genes responsible for mitochondrial biogenesis and mitochondrial autophagy (mitophagy). C57Bl/6 mice were treated with iron and/or lipopolysaccharide (LPS); N = 7 to 9 mice per group. Total RNA was extracted from mouse liver, and quantitative reverse transcription-polymerase chain reaction was performed using primers for Pgc-1α (a mitochondrial biogenesis-associated gene [A]), Ampk (a mitochondrial biogenesis-associated gene [B]), and Lc3b (a mitophagy-associated gene [C]). Lipopolysaccharide alone increases Lc3b mRNA levels, while decreasing Pgc-1α and Ampk mRNA levels. Iron-loaded mice stimulated with lipopolysaccharide had the opposite profile, with an increase in the mRNA levels of the mitochondrial biogenesis-associated genes Pgc-1α and Ampk (two-way ANOVA; interaction between iron and lipopolysaccharide not significant, therefore only main effects reported). Int = interaction P value.

Iron loading changes the balance between genes responsible for mitochondrial biogenesis and mitochondrial autophagy (mitophagy). C57Bl/6 mice were treated with iron and/or lipopolysaccharide (LPS); N = 7 to 9 mice per group. Total RNA was extracted from mouse liver, and quantitative reverse transcription-polymerase chain reaction was performed using primers for Pgc-1α (a mitochondrial biogenesis-associated gene [A]), Ampk (a mitochondrial biogenesis-associated gene [B]), and Lc3b (a mitophagy-associated gene [C]). Lipopolysaccharide alone increases Lc3b mRNA levels, while decreasing Pgc-1α and Ampk mRNA levels. Iron-loaded mice stimulated with lipopolysaccharide had the opposite profile, with an increase in the mRNA levels of the mitochondrial biogenesis-associated genes Pgc-1α and Ampk (two-way ANOVA; interaction between iron and lipopolysaccharide not significant, therefore only main effects reported). Int = interaction P value.

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