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(A,B) iTRAQ-based <t>proteomics</t> analysis. (A) Apoptosis promotors Casp9 , Casp8 , Bak1, and Dap were significantly down-regulated by YKL-40, while the apoptosis inhibitor Aven was significantly up-regulated. (B) Volcano Plot . Molecules down-regulated by YKL-40 are presented in the upper left area (green down arrow) while those up-regulated are shown in the upper right area (red up arrow), and those involved in apoptosis regulation are marked with up/down solid arrows. The most significant fold change ( FC ) on the expression level of these molecules was caused by Casp9 ( FC = 0.6411), followed by Aven ( FC = 1.3006). (C,D) Caspase-9 expression levels detected in BMDM and aorta tissues of Ldlr −/- mice. YKL-40 significantly down-regulated the activation level of caspase-9. (E) In RAW264.7, which was upregulated by Ykl-40 , the activation level of caspase-9 was significantly lower than that in control group ( p = 0.0054) while the expression level of Aven was significantly higher than in controls ( p = 0.0031). There was no significant difference in caspase-9 activation and Aven expression level between the Ykl40 downregulated group and normal controls ( p > 0.05). (F) Genetic expression relative fold changes of Casp9 , Dap , Aven and Bak1. No significant difference was indicated on Casp9 in BMDM after being treated by YKL-40 recombinant protein, but Aven was significantly up-regulated. (G) Casp9 , Aven expression levels were significantly upregulated in Ykl40 upregulated RAW264.7 ( p = 0.0154, p < 0.0001) and downregulated in the Ykl40 downregulated group ( p = 0.0039, p = 0.0037).
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(A,B) iTRAQ-based proteomics analysis. (A) Apoptosis promotors Casp9 , Casp8 , Bak1, and Dap were significantly down-regulated by YKL-40, while the apoptosis inhibitor Aven was significantly up-regulated. (B) Volcano Plot . Molecules down-regulated by YKL-40 are presented in the upper left area (green down arrow) while those up-regulated are shown in the upper right area (red up arrow), and those involved in apoptosis regulation are marked with up/down solid arrows. The most significant fold change ( FC ) on the expression level of these molecules was caused by Casp9 ( FC = 0.6411), followed by Aven ( FC = 1.3006). (C,D) Caspase-9 expression levels detected in BMDM and aorta tissues of Ldlr −/- mice. YKL-40 significantly down-regulated the activation level of caspase-9. (E) In RAW264.7, which was upregulated by Ykl-40 , the activation level of caspase-9 was significantly lower than that in control group ( p = 0.0054) while the expression level of Aven was significantly higher than in controls ( p = 0.0031). There was no significant difference in caspase-9 activation and Aven expression level between the Ykl40 downregulated group and normal controls ( p > 0.05). (F) Genetic expression relative fold changes of Casp9 , Dap , Aven and Bak1. No significant difference was indicated on Casp9 in BMDM after being treated by YKL-40 recombinant protein, but Aven was significantly up-regulated. (G) Casp9 , Aven expression levels were significantly upregulated in Ykl40 upregulated RAW264.7 ( p = 0.0154, p < 0.0001) and downregulated in the Ykl40 downregulated group ( p = 0.0039, p = 0.0037).

Journal: Frontiers in Cell and Developmental Biology

Article Title: YKL-40 Aggravates Early-Stage Atherosclerosis by Inhibiting Macrophage Apoptosis in an Aven-dependent Way

doi: 10.3389/fcell.2021.752773

Figure Lengend Snippet: (A,B) iTRAQ-based proteomics analysis. (A) Apoptosis promotors Casp9 , Casp8 , Bak1, and Dap were significantly down-regulated by YKL-40, while the apoptosis inhibitor Aven was significantly up-regulated. (B) Volcano Plot . Molecules down-regulated by YKL-40 are presented in the upper left area (green down arrow) while those up-regulated are shown in the upper right area (red up arrow), and those involved in apoptosis regulation are marked with up/down solid arrows. The most significant fold change ( FC ) on the expression level of these molecules was caused by Casp9 ( FC = 0.6411), followed by Aven ( FC = 1.3006). (C,D) Caspase-9 expression levels detected in BMDM and aorta tissues of Ldlr −/- mice. YKL-40 significantly down-regulated the activation level of caspase-9. (E) In RAW264.7, which was upregulated by Ykl-40 , the activation level of caspase-9 was significantly lower than that in control group ( p = 0.0054) while the expression level of Aven was significantly higher than in controls ( p = 0.0031). There was no significant difference in caspase-9 activation and Aven expression level between the Ykl40 downregulated group and normal controls ( p > 0.05). (F) Genetic expression relative fold changes of Casp9 , Dap , Aven and Bak1. No significant difference was indicated on Casp9 in BMDM after being treated by YKL-40 recombinant protein, but Aven was significantly up-regulated. (G) Casp9 , Aven expression levels were significantly upregulated in Ykl40 upregulated RAW264.7 ( p = 0.0154, p < 0.0001) and downregulated in the Ykl40 downregulated group ( p = 0.0039, p = 0.0037).

Article Snippet: iTRAQ-based proteomics analysis (Genechem Co.,Ltd., Shanghai, China) were performed to screen out the potential downstream target molecules of YKL-40.

Techniques: Expressing, Activation Assay, Recombinant