Lipid classes in human tissue sections from normal kidney tissue and clear-cell RCC tissue (CCRCC).

<p>All values are nmol/mg. Data are mean ± SEM.</p

VLDL-R expression is increased in clear-cell RCC.

<p>(<b>A</b>) Oil Red O staining of human tissue sections from normal kidney tissue (upper) and clear-cell RCC tissue (CCRCC; lower). (<b>B</b>) VLDL-R immunostaining (left) and quantification of immunostaining (right) of human tissue sections from normal kidney tissue (upper) and clear-cell RCC tissue (lower) (<i>n</i> = 6, *<i>p</i> = 0.0022). (<b>C</b>) Oil Red O staining (left) and quantification of staining (right) of cultured human cells isolated from healthy kidney tissue (upper) and clear-cell RCC tissue (lower) (<i>n</i> = 10, *<i>p</i> = 0.0058). (<b>D</b>) Quantification of VLDL-R mRNA normalized to 18S mRNA from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue (<i>n</i> = 6, *<i>p</i> = 0.004). (<b>E</b>) Quantification of immunoblot against VLDL-R with β-actin as loading control from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue (<i>n</i> = 6, *<i>p</i> = 0.0002). Data are shown as mean ± SEM.</p

VLDL-R overexpression in clear-cell RCC cells is mediated by HIF-1α, and promotes increased lipid accumulation through increased lipid uptake.

<p>(<b>A</b>) Quantification of VLDL-R mRNA normalized to 18S mRNA from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 10, *<i>p</i>≤0.05 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). (<b>B</b>) Quantification of immunoblot against VLDL-R with β-actin as loading control from cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 10, *<i>p</i>≤0.05 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). (<b>C</b>) Quantification of Oil Red O staining of cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 10, *<i>p</i>≤0.001 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). (<b>D</b>) Quantification of fluorescently internalized DiI-labeled lipoproteins in cultured human cells isolated from healthy kidney tissue and clear-cell RCC tissue treated with siRNA against HIF-1α or VLDL-R (<i>n</i> = 5, *<i>p</i>≤0.05 vs. control siRNA normal cells, †<i>p</i>≤0.05 vs. control siRNA clear-cell RCC cells). Data are shown as mean ± SEM.</p

Increased levels of ceramides in ischemic myocardium.

<p>Content of ceramide (A), sphingomyelin (B), phosphatidylcholine (C) and phosphatidylethanolamine (D), n = 7 per group. Results are shown as mean ± SEM, **<i>P</i><0.01 <i>vs.</i> control, ***<i>P</i><0.001 <i>vs.</i> control.</p

Increased expression of LDLr and LRP1.

<p><b>(A)</b> RT-QPCR analyses of mRNA expression of LDLr, VLDLr and SR-B1, n = 4 per group. <b>(B)</b> mRNA expression of VLDLr in HL-1 cells incubated in hypoxia for 0.5, 1, 6 and 24 h (n = 3). <b>(C)</b> Representative immunoblots of LDLr and LRP1. (D–E) Quantification of LDLr protein bands <b>(D)</b> and LRP1 protein bands <b>(E)</b> n = 6–7 per group. Results are shown as mean ± SEM, *<i>P</i><0.05 <i>vs.</i> control, **<i>P</i><0.01 <i>vs.</i> control, ***<i>P</i><0.001 <i>vs.</i> control.</p

Increased levels of cholesteryl esters in the pig myocardium.

<p><b>(A)</b> Content of cholesteryl esters, <b>(B)</b> triglycerides and <b>(C)</b> free cholesterol, n = 7 per group. Results are shown as mean ± SEM, ***<i>P</i><0.001 <i>vs.</i> control.</p