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. Author manuscript; available in PMC: 2018 Nov 22.
Published in final edited form as: Mol Psychiatry. 2017 Aug 29;23(9):1–11. doi: 10.1038/mp.2017.168

Figure 4. Alcohol exposure leads to lower PCSK9 expression in mice (a,b,c) and humans (d,e).

Figure 4

(a) PCSK9 mRNA expression in liver as a function of alcohol exposure status from mice that underwent the “NIAAA model of chronic and binge ethanol feeding”35 for 10-day chronic-plus-binge ethanol exposure. PCSK9 expression was significantly lower in the alcohol-exposed group (Student's t-test; Alcohol Exposure= 0.2443± 0.06553, No Alcohol Exposure= 1±0.07283, ****P<0.0001).

(b) PCSK9 protein expression in mouse liver was significantly higher in the control group compared to the case group that underwent the “NIAAA model of chronic and binge ethanol feeding”35 (Student's t-test; Alcohol Exposure= 0.2372± 0.01829, No Alcohol Exposure=0.4867 ± 0.0321, **P<0.01).

(c) Western blot of mouse liver PCSK9 levels as assessed by anti-PCSK9 antibody ab125251.

(d) Methylation analysis of PCSK9CpG1 in human alcohol-induced end-stage liver disease bulk tissue shows marked increase of methylation which might be due to general toxic effects of alcohol and end-stage organ disease. (Student's t-test; Alcohol Exposure= 46.19 ± 1.07, No Alcohol Exposure= 37.63 ± 0.8867, ****P< 0.0001).

(e) mRNA expression analysis of PCSK9 inhuman alcohol-induced end-stage liver disease bulk tissue reveals significantly decreased PCSK9 expression. (Student's t-test; Alcohol Exposure= 0.3517 ± 0.125, No Alcohol Exposure= 0.9992 ± 0.1388, **P< 0.01).