Capitalizing on the Autophagic Response for Treatment of Liver Disease Caused by Alpha-1-Antitrypsin Deficiency and Other Genetic Diseases
Figure 1
Accumulation of ATZ in liver specifically activates autophagy. Liver sections are stained with anti-GFP to enhance the fluorescent signal. (a) Sections from the GFP-LC3 mouse have GFP+ autophagosomes only in the starved state (right panel—starved for 24 h). (b) Sections from the Z × GFP-LC3 mouse have GFP+ autophagosomes; however, the mouse is fed, but only after doxycycline (Dox) is removed from the drinking water so that the ATZ gene is expressed (right panel). (c) Sections from the Saar × GFP-LC3 mouse (lower right) do not show autophagosomes when the AT Saar variant is expressed following withdrawal of Dox in the fed state, but starvation does lead to GFP+ autophagosomes (right panel). (d) GFP+ autophagosomes are present in the PiZ × GFP-LC3 mouse in the fed state, as this mouse has constitutive expression of ATZ. Reprint from reference [1] with permission.
