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Intermittent Hypoxia Induced Formation of "Endothelial Cell-Colony Forming Units (EC-CFUs)" Is Affected by ROS and
Katia Avezov1,2, Dror Aizenbud2, Lena Lavie1
1The Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Frontiers in Neurology
|July 3, 2018
Summary
Intermittent hypoxia increases endothelial cell colony-forming units (EC-CFUs) and their vascular functions via reactive oxygen species (ROS). Individual responses to hypoxia vary, suggesting potential clinical significance.
Area of Science:
- Cardiovascular Research
- Sleep Medicine
- Cell Biology
Background:
- Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH), leading to increased oxidative stress and endothelial dysfunction.
- Endothelial Cell-Colony Forming Units (EC-CFUs) serve as a marker for endothelial progenitor cells and reflect vascular repair mechanisms.
Purpose of the Study:
- To investigate the in vitro effects of IH and sustained hypoxia (SH) on EC-CFU development, function, and associated oxidative stress markers.
- To determine the role of reactive oxygen species (ROS) and NADPH-oxidase in IH-induced changes in EC-CFUs.
Main Methods:
- Blood samples from healthy volunteers were exposed to IH and SH conditions.
- EC-CFU numbers, area, proliferation, ROS production, and gene expression (NADPH-oxidase, VEGF, Nrf2) were analyzed.
- Paracrine effects on endothelial tube formation were assessed, with ROS and NADPH-oxidase inhibition used to probe mechanisms.
Main Results:
- IH significantly increased EC-CFU numbers and VEGF and gp91phox expression, with notable inter-individual variability.
- ROS production and oxidative stress markers were elevated under IH, while Nrf2 expression and colony size remained unchanged.
- Conditioned media from IH/SH-treated EC-CFUs enhanced endothelial tube formation, an effect reduced by antioxidants and NADPH-oxidase inhibitors.
Conclusions:
- IH-induced oxidative stress, mediated by ROS, enhances EC-CFU vascular and paracrine capacities.
- The significant inter-individual variability in EC-CFU response to IH suggests a potential clinical trait relevant to OSA.
- ROS play a crucial role in mediating the adaptive responses of EC-CFUs to hypoxic conditions.