Figure 7 (See previous page).
Defective VSMC autophagy promotes neointima formation 5 wk after ligation-induced injury. (A,B) The left common carotid artery (LCCA) of Atg7+/+Tagln-Cre+ (+/+) (n = 10) and Atg7F/FTagln-Cre+ (−/−) mice (n = 12) was ligated for 5 wk. Sections of the LCCA were stained with anti-ACTA2 antibody (A) or Sirius red (B) to quantify the degree of stenosis and total collagen deposition, respectively. Scale bar: 100 µm. (**P < 0.01; *P < 0.05; Student t test). (C) Sections of the LCCA were immunostained for CDKN2A to quantify CDKN2A-positive nuclei (black arrowheads). Scale bar: 25 µm. (**, P < 0.01; Mann Whitney test). (D) The LCCA was stained for senescence-associated GLB1 activity ex vivo (right panel). Scale bar: 250 µm. Sections of the LCCA were then counterstained with periodic acid-Schiff (PAS) to identify senescent neointimal VSMCs (left panel). Note that the neointimal VSMCs are surrounded by a cage of PAS-positive basal lamina. Scale bar: 10 µm.