Journal: JVS-vascular science
Article Title: Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury
Figure Lengend Snippet: Canonical transient receptor potential 6 deficient ( TRPC6 −/− ) SMC are phenotypically modulated in culture and in situ. A-C , Lysates were prepared from cultured wild-type (WT) and TRPC6 −/− VSMC (passages 6–8), resolved by sodium dodecyl sulfate polyacrylamide gel electrophoresis, and immunoblotted for SM22 and MYH11. Actin served as the loading control. A , Representative immunoblot. B and C , Relative MYH11 and SM22 protein expression quantified by densitometry (n = 3 immunoblots). D , Immunohistochemistry (IHC) performed on common carotid artery (CCA) cross-sections of 8- to 10-week-old male WT and TRPC6 −/− mice. (Top) IHC for SM22 and (Bottom) MYH11. E , SM22 protein levels were assessed at passages 1, 4, and 7 in WT and TRPC6 −/− VSMC by immunoblot analysis and quantified by densitometry. F and G , Lysates were prepared from cultured WT and TRPC6 −/− VSMC (passages 6–8) and immunoblotted for beta-actin and GAPDH. F , Representative western blot. G , The ratio of beta actin to GAPDH protein was quantified by densitometry (n = 3). H and I , Relative MYH11 and SM22 mRNA levels were assessed by quantitative real-time PCR in cultured WT and TRPC6 −/− VSMC (passages 6–8; n = 4).
Article Snippet: TRPC6 −/− VSMC show increased proliferation and migration as well as decreased contractile biomarker expression.
Techniques: In Situ, Cell Culture, Polyacrylamide Gel Electrophoresis, Expressing, Western Blot, Immunohistochemistry, Mouse Assay, Real-time Polymerase Chain Reaction