VLDL Induced Modulation of Nitric Oxide Signalling and Cell Redox Homeostasis in HUVEC

Figure 1

Gene expression changes induced by VLDL. HUVEC were incubated 24 h with n-VLDL (grey) or ox-VLDL (black), both 140 μg/mL. cDNA were assayed by RT-PCR (Human Nitric Oxide Signalling Pathway RT² Profiler PCR Array). The relative expression of the genes of interest is shown. (a) Endothelial nitric oxide synthase (eNOS). (b) Inducible nitric oxide synthase (iNOS). (c) Genes involved in the regulation of eNOS activity. (i) HSP90AB1: heat shock protein 90 kDa α (cytosolic), class B member 1; (ii) GLA: galactosidase α; (iii) GCH1: GTP cyclohydrolase 1; (iv) GCHFR: GTP cyclohydrolase I feedback regulator; (v) DDAH2: dimethylarginine dimethylaminohydrolase 2; (vi) ARG2: arginase, type II. (d) Genes induced by nitric oxide and involved in superoxide metabolism/oxidative stress response. (i) IL8: interleukin 8; (ii) VEGFA: vascular endothelial growth factor A; (iii) SOD1: superoxide dismutase 1, soluble; (iv) SOD2: superoxide dismutase 2, mitochondrial; (v) NCF2: neutrophil cytosolic factor 2; (vi) NQO1: NAD(P)H dehydrogenase, quinone 1; (vii) ALOX12: arachidonate 12-lipoxygenase, 12S type. Relative expression calculated after β-actin normalisation versus control cells. Data ± SD; n. of biological experiments = 3. values were considered statistically significant by ANOVA.

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