Oxidative Medicine and Cellular Longevity / 2018 / Article / Fig 5

Research Article

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

Figure 5

mROS scavenging with MitoTEMPO restores endothelial responses to Bk (a–d). In order to evaluate whether PTH-dependent ROS production is responsible of the endothelial dysfunction, we tested endothelial responsiveness to both Bk and Ach in the presence of a selective mROS scavenger (MitoTEMPO). BAECs were pretreated with MitoTEMPO (5 μM), stimulated with PTH (0.1 nM) 30 minutes later and after 24 hours, both Ca2+ kinetics and NO release were assessed in response to either Bk (30 nM) (a–b) or Ach (1 μM) (c–d), as described in Materials and Methods. 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 either Bk or Ach; 0 = fluorescence signal of unstimulated BAECs). All images are the mean of three independent experiments.
(a)
(b)
(c)
(d)