FIGURE 3.

SDC4 KO promoted CaCl₂‐induced abdominal aortic aneurysm (AAA) formation. (A) Representative images showing the morphology of CaCl₂‐induced AAAs. (B and C) The AAA incidence (B) and survival curve (C) of wild‐type (WT) mice stimulated with CaCl₂ (n = 15) compared with that of SDC4‐/‐mice (n = 15). No AAA developed in saline‐treated mice (n = 10). (D) The maximal abdominal aortic diameter in CaCl₂‐ and saline‐treated mice. (E and F) Representative images of H&E staining (E), elastica van Gieson (EVG) staining and the elastin degradation score (F) of abdominal aortas from CaCl₂‐ and saline‐treated mice (n = 5) (scale bars, 300 μm and 100 μm) (magnified photographs). (G) Immunohistochemical analysis of α‐SMA positive cells in SDC4‐/‐ and WT mice after CaCl₂ or saline treatment (scale bars, 25 μm). (H) Representative western blots of MMP9 and MMP2 and densitometric analysis of saline‐ and CaCl₂‐treated mice (n = 5). (I) Representative western blots of α‐SMA, Calponin1 and SM‐MHC and densitometric analysis of saline‐ and CaCl₂‐treated mice (n = 5). (J) The level of reactive oxygen species (ROS) in the abdominal aortas of CaCl₂‐ and saline‐infused mice was evaluated by dihydroethidium (DHE) staining and quantified by determining the ratio of DHE‐positive cells (n = 5) (scale bars, 500 μm and 100 μm) (magnified photographs)