Skip to main content
. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Jan 8;35(3):535–546. doi: 10.1161/ATVBAHA.114.304029

Figure 4. Maintaining MYOCD expression prevents and reverses phenotypic changes in VSMC associated with cholesterol loading.

Figure 4

(A) Shown is immunostaining of mouse VSMC transduced with adenoviral vectors (MOI of 300) expressing either MYOCD (Ad-MYOCD) or LacZ (Ad-LacZ) prior to incubation with CD-cholesterol complexes for 72 hours (40×). Note the persistence of ACTA2 and the lack of CD68 in Ad-MYOCD vs. Ad-LacZ cells. (B–C) qRT-PCR analysis of mRNA from cells treated as in (A) showed an adenoviral vector-dose related maintenance and suppression, respectively, of VSMC marker Cnn1 and of macrophage marker Cd68. (D–E) Mouse VSMC were transduced with Ad-MYOCD or Ad-LacZ (MOI of 300) after 3 days of cholesterol loading. qRT-PCR results show increases of Cnn1 (D) and Srf mRNA (E), and suppression of Cd68 mRNA (E) in Ad-MYOCD cells (*p < 0.05; data shown are mean ± SD of triplicates of qRT-PCR reactions and are representative of two independent experiments).