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. 2024 Mar 30;15:2789. doi: 10.1038/s41467-024-46336-2

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — a Experimental scheme demonstrating that PCSK9 aggravated atherosclerosis in Cap1^+/+ versus Cap1^+/− mice. AdV-PCSK9 (1 × 10¹¹ infectious units/mouse) was intravenously administered to mice on a high-fat diet. b Plasma hPCSK9 levels were measured using ELISA in Cap1^+/+ (AdV-CTRL N = 4; AdV-PCSK9 N = 9) and Cap1^+/− (AdV-CTRL N = 4; AdV-PCSK9 N = 12) mice with or without PCSK9 overexpression. The plasma hPCSK9 concentration in the AdV-CTRL group was 12–14 ng/mL, whereas it was 30–50% higher in the AdV-PCSK9 group. c Oil Red O staining of carotid arteries after AdV-CTRL or AdV-PCSK9 injection into Cap1^+/+ (AdV-CTRL N = 7; AdV-PCSK9 N = 18) and Cap1^+/− (AdV-CTRL N = 8; AdV-PCSK9 N = 14) mice. The atherosclerotic plaque area in the D-flow arteries increased after PCSK9 administration in Cap1^+/+ mice, which was prevented in Cap1^+/− mice. The scale bar represents 2 mm. d qPCR analysis demonstrating pro-inflammatory molecules in S-flow or D-flow arteries from Cap1^+/+ versus Cap1^+/− mice. Expression of TNF-α, IL-1β, and IL-6 was higher in D-flow than in S-flow arteries (P < 0.001, P = 0.004, and P = 0.023, respectively) in Cap1^+/+ mice with a high serum level of PCSK9. However, induction of inflammatory cytokines under D-flow was prevented in Cap1^+/− mice (P = 0.002, 0.007, 0.029, respectively) (N = 3). e H&E staining of S-flow or D-flow arteries (from the aortic root at 0.3, 0.6, and 1 mm, respectively) from Cap1^+/+ versus Cap1^+/− mice with AdV-CTRL or AdV-PCSK9. In the presence of a high serum level of PCSK9, significant atherosclerotic plaques developed under D-flow in Cap1^+/+ mice, which was prevented in Cap1^+/− mice. The scale bar represents 200 μm. f Masson’s trichrome and Oil red O staining. Each scale bar represents 200 μm, and 50 μm (magnified fields). g Immunofluorescence images stained with TUNEL (green). The bottom panel displays a magnified view, specifically highlighting the arteries exposed to low shear stress from the AdV-PCSK9 group. The scale bar represents 100 μm (top), 25 μm (mid) and 20 μm (enlarged). The differences between the groups were compared using the unpaired t-test (two-tailed). All experiments are independently performed. Data are presented as mean values ± SEM and SD (in (b, d) only).