AI Article Synopsis
- Patients with obstructive sleep apnoea (OSA) face significant damage to their blood vessels, primarily due to a condition called chronic intermittent hypoxia (CIH).
- The study examined how CIH impacts human vein endothelial cells by monitoring cell health, mitochondrial function, and specific protein expressions.
- Findings revealed that CIH led to decreased cell viability and increased cell death, but treatments with certain drugs improved cell survival and mitochondrial health, indicating that a protein called PPARγ plays a critical role in these protective processes.
Article Abstract
Purpose: Patients with obstructive sleep apnoea (OSA) have a high incidence of vascular endothelial injury. The most important pathophysiological feature of OSA is chronic intermittent hypoxia (CIH). This study aimed to investigate the mechanisms of CIH-related vascular endothelial injury.
Methods: IH exposure was applied to human umbilical vein endothelial cells (HUVECs). After modeling, cell viability, the expression levels of peroxisome proliferator activated receptor γ (PPARγ), apoptosis-associated proteins and mitochondrial division fusion proteins, and the levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were assessed via Cell Counting Kit-8 (CCK-8), western blotting, fluorescent microscope, and flow cytometry, respectively. Rosiglitazone (PPARγ agonist), tempo (the mitochondrial-specific antioxidant), and tempo combined with PPARγ interfering RNA were used to treat HUVECs, respectively.
Results: After IH exposure, cell viability and levels of MMP decreased, cell apoptosis and ROS levels increased, and the expression levels of PPARγ decreased. Both tempo and rosiglitazone pretreatment ameliorated cell apoptosis and improved cell viability. In addition, mitochondrial function became better after tempo pretreatment. PPARγ interference reversed the protective effects of tempo on IH-related mitochondrial function injury and cell injury.
Conclusions: PPARγ regulated the apoptosis and cell viability of IH-treated HUVECs by altering mitochondrial function. This finding clarifies the mechanism of CIH-related vascular endothelial injury.
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| http://dx.doi.org/10.1007/s11325-022-02696-x | DOI Listing |
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