Fig 1: Addition of LXRa agonist (A) T0901317 or (B) 22R-HC normalized IDOL and (C and D) reduced LDLR expression, respectively, in atorvastatin-treated THP-1 cells. Each bar represents the mean and SD of triplicate experiments. *P < 0.05 compared to non-treated cells, # P < 0.05 compared to atorvastatin-treated cells. The statistical significance of differences was determined using ANOVA followed by Bonferroni’s comparison.
Fig 2: LDLR c.2160delC variant affected the expression of LDLR. (A) The mRNA expression level of LDLR c.2160delC in HEK293T cells. (B) The protein expression of LDLR c.2160delC in HEK293T cells. (C) LDLR expression on the HEK293T cell surface. **** represents P < 0.01
Fig 3: Pathogenic variants and in silico analysis. (A) The results of whole-exome sequencing. (B) Sanger sequencing confirmed the existence of LDLR c.2160delC. The reverse primer was used for Sanger sequencing. The shaded area represents the actual base. The contents of the box are the stop codon induced by the deletion mutation of the 2160 locus
Fig 4: Representative confocal microscopy images of the localization of LDLR in the endoplasmic reticulum. Blue fluorescence represents the endoplasmic reticulum, while red fluorescence represents LDLR
Fig 5: Antibody-mediated inhibition of LDLR blocks S protein pseudovirion infection of ARPE-19 cells. (A). LDLR is expressed in ARPE-19 cells; immunoblot visualized with anti-LDLR antibody (*; red). (B). Fold difference in uptake of original spike-pseudotyped lentiviruses at MOI 10 in the presence of anti-LDLR antibody at 1:500 dilution (1 µg/mL) and 1:250 dilution (2 µg/mL) at 24 h compared to untreated controls infected with original spike protein pseudotyped particles alone. * p < 0.01, ** p < 0.001, **** p < 0.0001.
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