Parathyroid Hormone Causes Endothelial Dysfunction by Inducing Mitochondrial ROS and Specific Oxidative Signal Transduction Modifications

Figure 2

PTH spares endothelial responses to acetylcholine (Ach) (a–d). BAECs were treated with PTH (0.1 nM) for 24 hours, and Ca²⁺ fluxes were assessed in response to Ach (1 μM), incubating the cells with the fluorescent probe Fluo4-AM. The fluorescence intensity was determined by a microplate fluorescence reader. The fluorescent signal was corrected for the background signal derived from nonmarked cells. All data are reported as –₀ ( = fluorescence signal of BAECs stimulated with Ach; ₀ = fluorescence signal of BAECs at basal condition) (a). Peak of cytosolic Ca²⁺ is reported as fold changes vs. controls, whose mean value was set as 1 (b). BAECs were treated with PTH (0.1 nM) for 24 hours, and NO release was assessed in response to Ach (1 μM), incubating the cells with the fluorescent probe DAF-FM diacetate. The fluorescence intensity was determined by a microplate fluorescence reader. The fluorescence was corrected by the background signal derived from nonmarked cells. All data are reported as –₀ ( = fluorescence signal of BAECs stimulated with Ach; ₀ = fluorescence signal of unstimulated BAECs) (c). Peak of NO release was reported as fold changes vs. controls, whose mean value was set as 1 (d). All images are the mean of three independent experiments.

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