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. 2009 Oct 27;18(2):317–326. doi: 10.1038/mt.2009.249

Figure 4.

Figure 4

Functional complementation of LDLR deficiency in CHO a7 Ldlr−/− cell lines and familial hypercholesterolemia (FH) primary patient cells. (a) Incubation of Chinese hamster ovary (CHO) a7 Ldlr−/− cells with fluorescently labeled low-density lipoprotein (LDL) (DiI-LDL) after transduction with pEHHZ-LDLR-LDLR confirmed expression of functional LDL receptor (LDLR) from the plasmid. (b) Transduction of CHO a7 Ldlr−/− with pEHHZ-LDLR-LDLR resulted in functional complementation of the LDLR deficiency under physiological regulation. (c) Transduction of FH primary patient fibroblasts with pEHHZ-LDLR-LDLR led to functional complementation of LDLR deficiency under physiological regulation. Cells were transduced at a multiplicity of infection of 10 and expression was assayed 48–72 hours post-transduction. Luciferase data are normalized to O-nitrophenyl-β-galactopyranoside (ONPG) to control for differences in vector transduction. Means are from three independent experiments each repeated in quadruplicate. Results are mean ± SD.