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. 2013 Jul 2;18(1):118–129. doi: 10.1016/j.cmet.2013.06.003

Figure 2.

Figure 2

Cold-Induced Atherosclerotic Plaque Growth and Instability in ApoE−/− Mice and Ldlr−/− Mice

(A) Gross examination and quantification of the general oil red O-stained aorta stem from ApoE−/− mice exposed to 4°C and 30°C. (n = 10/group).

(B) Cross-section histological analysis and quantification of aorta roots exposed to 4°C and 30°C for 8 weeks by staining with H&E, oil red O, MOMA-2, α-SMA, or Sirius red. Nonimmune IgG was used as negative control. Dashed lines encircle some parts of atherosclerotic plaques, and arrowheads in different panels point to positive signals (n = 10/group).

(C) Dashed lines encircle the necrotic core area. nec, necrotic core.

(D) Quantification of average necrotic core areas, the ratio of the necrotic core area versus the aortic root plaque area, and the fibrous cap thickness in groups exposed to 4°C and 30°C (n = 10/group).

(E) Metabolic rate of O2 consumption and CO2 production in response to NE in Ldlr−/− mice (n = 6–7/group).

(F) Blood chemistry analysis of TG, cholesterol, and LDL levels (n = 8/group). FPLC analysis of plasma cholesterol and TG in pair-fed Ldlr−/− mice exposed to 4°C and 30°C (n = 5/group).

(G) Measurement of cAMP and glycerol release in eWAT of Ldlr−/− mice exposed to 4°C and 30°C for 8 weeks (n = 4–5/group).

(H) Quantification of plaque area and histological analysis of atherosclerotic plaques of aortic root in Ldlr−/− mice exposed to 4°C and 30°C (n = 10/group). Tho.A, thoracic artery; Abd.A, abdominal artery; C.I.A, common iliac artery.