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Fig. 3 | Arthritis Research & Therapy

Fig. 3

From: Role of endoplasmic reticulum stress in the protective effects of PPARβ/δ activation on endothelial dysfunction induced by plasma from patients with lupus

Fig. 3

Effects of PPARβ/δ activation on endothelial nitric oxide (NO) production. NO production was stimulated by the calcium ionophore A23187 (a) in human umbilical cord vein endothelial cells (HUVECs) incubated in plasma from patients with systemic lupus erythematosus (SLE) with active nephritis (AN) or healthy controls (Ctrol), or in plasma from patients with antiphospholipid syndrome (APS) (b), in the presence and/or in absence of GW0742 and GSK0660. Values are expressed as mean ± SEM (n = 5–6). c Expression of PPARβ/δ at the level of mRNA expression by real time RT-PCR and protein by western blot in HUVECs transfected with either PPAR-β-specific siRNA (siRNA-PPAR-β) or empty vector (siRNA-control). Data are presented as gene expression normalized to Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) levels or densitometric protein band and normalized to the corresponding β-actin. Results are representative of six independent experiments. ** P < 0.05 vs siRNA-control. d A23187-mediated NO production in control siRNA and siRNA-PPAR-β cells incubated in plasma from patients with AN-SLE or Ctrol for 24 h, in the presence or absence of GW0742 (1 μmol/L). All data are mean ± SEM (n = 8). NO release was estimated from the area under the curve (AUC) of the fluorescent signal of 4,5-diaminofluorescein (DAF-2) for 30 min of stimulation. ** P < 0.01 vs Ctrol. ## P < 0.01vs without PPAR agonist. + P < 0.05 vs GW0742 column. δδ P < 0.01 vs Ctrol siRNA-control column

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