Abstract
Endothelial cells (ECs) are exposed to molecular dioxygen and its derivative reactive oxygen species (ROS). ROS are now well established as important signaling messengers. Excessive production of ROS, however, results in oxidative stress, a significant contributor to the development of numerous diseases. Here, we analyze the experimental data and theoretical concepts concerning positive pro-survival effects of ROS on signaling pathways in endothelial cells (ECs). Our analysis of the available experimental data suggests possible positive roles of ROS in induction of pro-survival pathways, downstream of the Gi-protein-coupled receptors, which mimics insulin signaling and prevention or improvement of the endothelial dysfunction. It is, however, doubtful, whether ROS can contribute to the stabilization of the endothelial barrier.
Highlights
Cells of vasculature, red blood cells (RBCs), endothelial cells (ECs), and vascular smooth muscle cells (VSMCs), work in concert to match the oxygen supply with tissue oxygen demand [1]
reactive oxygen species (ROS) derived from NOX1 and NOX4 are important regulators of proliferation, hypertrophy and apoptosis in human pulmonary artery endothelial and smooth muscle cells, which can lead to airway and vascular remodeling
The aim of this review was to analyze the literature evidence to test our hypothesis that ROS can evoke beneficial effects on ECs
Summary
Cells of vasculature, red blood cells (RBCs), endothelial cells (ECs), and vascular smooth muscle cells (VSMCs), work in concert to match the oxygen supply with tissue oxygen demand [1]. There is experimental evidence for activation of these pro-survival pathways by Gi -protein-coupled receptors (Gi -PCRs) via liberation and activation of the. Gβγ, which can be activated due to ROS-induced activation of Gαi (Nishida) [24,25] is likely to activate the PI3K–Akt pathway in a receptor-independent manner, and promote EC survival (Figure 1). In HUVECs, stimulation of cannabinoid receptors (CB1 and CB2 are both coupled to Gi/o proteins [30]) by anandamide, induced apoptosis via activation of the JNK and p38 MAPK [31]. In human coronary artery ECs (HCAECs), stimulation of the CB1 receptor led to apoptosis via increase in ROS generation and activation of JNK and p38 MAPKs [32]
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