Hypoxia increases atorvastatin-induced decay-accelerating factor expression

<p><b>Copyright information:</b></p><p>Taken from "Statin-induced expression of CD59 on vascular endothelium in hypoxia: a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis"</p><p>Arthritis Research & Therapy 2006;8(4):R130-R130.</p><p>Published online 21 Jul 2006</p><p>PMCID:PMC1779384.</p><p></p> Analysis of decay-accelerating factor expression on human umbilical vein endothelial cells (HUVEC) following 48 hours culture in 21% O(open bars) or 1% O(filled bars) in the presence or absence of atorvastatin (0.25 μM). and HUVEC were treated with increasing concentrations of atorvastatin for 48 hours in the presence (filled bars) or absence (open bars) of (b) cobalt chloride (CoCl) (100 μM) or (c) desferrioxamine (DFO) (100 μM). Decay-accelerating factor expression was measured by flow cytometry using the mAb 1H4. Bars represent the mean ± standard error of the mean (= 4). *< 0.05, **< 0.01 compared with untreated controls

Mechanisms involved in atorvastatin-induced decay-accelerating factor expression

<p><b>Copyright information:</b></p><p>Taken from "Statin-induced expression of CD59 on vascular endothelium in hypoxia: a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis"</p><p>Arthritis Research & Therapy 2006;8(4):R130-R130.</p><p>Published online 21 Jul 2006</p><p>PMCID:PMC1779384.</p><p></p> Human umbilical vein endothelial cells (HUVEC) were cultured for 48 hours under hypoxia (1% O) and were treated with atorvastatin (At) (0.5 μM) in the presence or absence of mevalonate (200 μM), -monomethyl-L-arginine (L-NMMA) (500 μM), -nitro-L-arginine methyl ester (L-NAME) (100 μM) and geranylgeraniol (GGOH) (20 μM). Endothelial cell CD59 expression was measured by flow cytometry using the mAb BRIC 229. Results are expressed as the percentage increase in relative fluorescence intensity above the hypoxic control (US) (= 4). *< 0.5, **< 0.01 compared with untreated controls

Atorvastatin-induced CD59 and decay-accelerating factor in hypoxia enhance endothelial cell cytoprotection

<p><b>Copyright information:</b></p><p>Taken from "Statin-induced expression of CD59 on vascular endothelium in hypoxia: a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis"</p><p>Arthritis Research & Therapy 2006;8(4):R130-R130.</p><p>Published online 21 Jul 2006</p><p>PMCID:PMC1779384.</p><p></p> Human umbilical vein endothelial cells (HUVEC) were cultured under normoxic or hypoxic conditions with and without atorvastatin (0.25 μM) for 48 hours followed by 3 hours reoxygenation. Harvested endothelial cells (EC) were incubated with 20% C5-deficient (C5 D) serum (filled bars) or heat-inactivated (HI) normal human serum (NHS) (open bars) for 2 hours. C3 binding was analysed by flow cytometry and results are expressed as the percentage of C3 binding relative to that on EC exposed to C5 D in normoxia (shown as 100%). *< 0.05 (= 4), difference between levels of cell surface C3 deposition on EC cultured under hypoxic conditions in the presence or absence of atorvastatin HUVEC were cultured under normoxic or hypoxic conditions with and without atorvastatin (0.5 μM) for 48 hours followed by 3 hours of reoxygenation. C9 binding was analysed by flow cytometry following incubation with 20% NHS (filled bars) or HI serum (open bars). Results are expressed as the percentage of C9 binding relative to that on EC exposed to NHS in normoxia (shown as 100%). *< 0.05 (= 4), difference between statin-treated and untreated EC in hypoxia.HUVEC were incubated in 1% Owith or without atorvastatin (At) 0.5 μM for 48 hours followed by 3 hours of reoxygenation. EC were preincubated with the inhibitory mAbs Bric229 (CD59) and 1H4 (decay-accelerating factor) (20 μg/ml) or veronal buffered saline + 1% gelatin at 4°C. EC were then incubated with 20% rabbit serum or 20% HI rabbit serum at 37°C for 1 hour and propidium iodide (PI) was added prior to analysis by flow cytometry. The percentage EC lysis was calculated as the number of PI-positive cells expressed as a percentage of the total number of cells. **< 0.001 (= 4), difference between statin-treated and untreated EC