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

Figure 1

PTH impairs endothelial responses to bradykinin (Bk) (a–e). BAECs were treated with PTH (0.1 nM) for 24 hours, and Ca²⁺ fluxes were assessed in response to Bk (30 nM), incubating the cells with the fluorescent probe Fluo4-AM. 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 Bk; ₀ = fluorescence signal of unstimulated BAECs) (a). Peak of cytosolic Ca²⁺ was reported as fold changes vs. controls, whose mean value was set as 1 ( vs. CTRL) (b). Plateau of Ca²⁺ kinetics in response to Bk was evaluated as area under the curve (AUC) of the plateau phase (starting from 100 seconds and up to 200 seconds after Bk administration). Data are reported as fold changes vs. controls, whose mean value was set as 1 ( vs. CTRL) (c). BAECs were treated with PTH (0.1 nM) for 24 hours, and NO release was assessed in response to Bk (30 nM), 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 Bk; ₀ = fluorescence signal of unstimulated BAECs) (d). Peak of NO release was reported as fold changes vs. controls, whose mean value was set as 1 ( vs. CTRL) (e). All images are the mean of three independent experiments.

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