Fig. 6: Elevated CUX1 and p16INK4a expression in plaque zones from patients with carotid artery disease.
From: Post-GWAS functional analysis identifies CUX1 as a regulator of p16INK4a and cellular senescence
a,b, qPCR showing significant increase in expression of CUX1 (P = 0.036) (a) and p16INK4a (P = 0.011) (b) in plaque versus normal-appearing zones obtained from patients with carotid artery atherosclerosis. Data for qPCR analysis represent n = 11 plaque zones and n = 9 normal-appearing zones. c,d, Nonparametric Spearman correlation analysis (c) and trend analysis (d) showing significant correlation between the expression levels of CUX1 and p16INK4a (P = 0.047 and P = 0.005, respectively; n = 13). e, Immunocytochemical staining with antibodies specifically against CUX1 (green) and p16INK4a (red) in plaque and normal-appearing zones from patients with carotid artery atherosclerosis. Data were generated by staining of n = 8 plaque zone and n = 8 normal-appearing zones in two independent experiments. DAPI (blue) was applied to stain fixed cells. f, Statistical analysis of immunocytochemical staining showing significant induction of CUX1 (P = 0.0025) and p16INK4a (P = 0.0006) in plaque zones compared to normal-appearing zones. g, qPCR showing a trend of increase with no statistical significance in the expression of SASP genes IL-6 (left; P = 0.502), IL-1β (middle; P = 0.255) and ICAM1 (right; P = 0.17). Data for qPCR analysis represent n = 11 plaque zones and n = 9 normal-appearing zones. a–d,g, Data presented as mean ± s.e. P values were calculated using two-tailed Student’s t-test. f, Non-normally distributed data are presented as median ± interquartile range, and P values were calculated with the nonparametric Mann–Whitney test.
