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. Author manuscript; available in PMC: 2010 Dec 1.
Published in final edited form as: Cell Signal. 2009 Aug 23;21(12):1874–1884. doi: 10.1016/j.cellsig.2009.08.003

Figure 7.

Figure 7

Effect of Mx1Cre-mediated conditional knock out of PPARγ on AGP-induced neointima. Panel A: Trichrome staining of a representative Mx1Cre transgenic mouse carotid three weeks after exposure to 2.5 μM AGP. Panel B: Representative trichrome-stained carotid of a pIpC-induced PPARγfl/− mouse three weeks after AGP treatment. Panel C: Trichrome-stained mouse carotid from a Mx1CreXPPARγfl/− mouse without pIpC induction three weeks after exposure to 2.5 μM AGP. Panel D: Trichrome-stained carotid from a pIpC-induced ΔPPARγ mouse three weeks after AGP treatment. Note the complete lack of neointima development. Panel E: Anti-αSMA staining of an uninduced Mx1CreXPPARγfl/− mouse three weeks after AGP treatment. Note the αSMA positive neointimal cells inside the internal elastic lamina (IEL) that shows red autofluorescence. EEL- external elastic lamina. Panel F: Anti-αSMA staining of an pIpC-induced ΔPPARγ mouse three weeks after AGP treatment. Note the complete lack of αSMA staining inside the IEL. Calibartion bars are 100 μm. Intima to media ratios in mice with or without pIpC induction three weeks after exposure to 2.5 μm AGP (panel G) or ROSI (panel H). Asterisks denote significant differences to uninduced vehicle-treated Mx1CreXPPARγfl/− mice (p< 0.05, n= 5–10 mouse per group).