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. 2015 Mar 24;112(14):4447–4452. doi: 10.1073/pnas.1420363112

Fig. 3.

Fig. 3.

Myocd deletion triggers autophagy in SMCs populating the aorta. (A–J) Immunohistochemical analysis performed on aortic sections harvested 14 d following tamoxifen treatment of MyocdF/F control (A–E) and SMMHC-CreERT2/MyocdF/F mutant mice (F–J) reveals marked induction of Beclin-1 (green), ATG7 (green), ATG5 (green), LC3 (green), and p62 (green) in medical SMCs of SMMHC-CreERT2/MyocdF/F mutant mice. Original magnification, 400× (A and F) and 200× (B–E and G–J). (K) qRT-PCR demonstrating 3–10-fold induction of genes encoding ATG5, ATG7, Beclin-1, LC3a, and LC3b in tamoxifen-treated SMMHC-CreERT2/MyocdF/F mutant mice (red bars) compared with MyocdF/F control mice (black bars). Data are expressed as mean gene expression (arbitrary units) ± SEM. (L) Representative ethidium bromide-stained agarose gel showing relative levels of autophagy-related gene expression in qRT-PCR amplified mRNA harvested from tamoxifen-treated MyocdF/F (Con) and SMMHC-CreERT2/MyocdF/F mutant (Mut) mice. (M–P) Electron micrographs of aortic SMCs harvested 14 d following tamoxifen treatment of SMMHC-CreERT2/MyocdF/F mutant mice. As anticipated, abundant myofibers and mitochondria (arrows) in MyocdF/F control vascular SMCs (M and N). By contrast, evidence of cellular stress (vacuoles) and autophagosomes (arrows) was observed in the cytoplasm of SMCs populating the aorta of SMMHC-CreERT2/MyocdF/F mutant mice (O and P). Original magnification, 50,000×.