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Decreased expression of PPARγ is associated with aortic endothelial cell apoptosis in intermittently hypoxic rats
Ningfang Lian1, Mengxue Chen1, Shuyi Zhang1
1Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China.
Purpose:
Increasing medical researche shows that endothelial dysfunction is one of the important causes of various cardiovascular diseases related to chronic intermittent hypoxia (CIH). This study aimed to identify target proteins in CIH-related vascular dysfunction.
Methods:
A comparative proteomics analysis was conducted in aortic samples of rats treated with CIH and controls with normoxia. Bioinformatics analyses were performed to determine the potential roles of major proteins. The expressions of target proteins were measured by western blotting. Cell apoptotic ratio was detected by flow cytometer.
Results:
A total of 3,593 proteins in aortic tissues of rats were quantified. Ninety-two upregulated proteins and 468 downregulated proteins were identified when the cutoff of fold change was set at 1.5 (CIH vs. normoxia). The results of bioinformatics analysis revealed that the differentially expressed proteins were enriched in the processes of energy metabolism and lipid metabolism. The reduced expression level of peroxisome proliferator-activated receptor γ (PPARγ) protein was identified in thoracic aortic tissues of rats with CIH by proteomics analysis and western blotting. In intermittent hypoxia-treated rat aortic endothelial cells, PPARγ protein levels were reduced, and the apoptosis rate and caspase-3 and Bax protein levels were markedly elevated. Importantly, forced expression of PPARγ by rosiglitazone in intermittent hypoxia-treated rat aortic endothelial cells not only attenuated caspase-3 and Bax protein levels but also reduced the rate of apoptosis.
Conclusion:
PPARγ is critical in endothelial dysfunction of rats with CIH. Additional studies on these differentially expressed proteins associated with CIH-related endothelial dysfunction are necessary.
Insights
Chronic intermittent hypoxia (CIH) causes endothelial dysfunction. This study identified reduced peroxisome proliferator-activated receptor gamma (PPARγ) as a key factor in CIH-related vascular issues.
Area of Science:
- Cardiovascular Research
- Proteomics
- Molecular Biology
Background:
- Endothelial dysfunction is a significant contributor to cardiovascular diseases linked to chronic intermittent hypoxia (CIH).
- Identifying specific molecular targets is crucial for understanding and treating CIH-related vascular dysfunction.
Purpose of the Study:
- To identify key proteins involved in vascular dysfunction caused by chronic intermittent hypoxia (CIH).
- To investigate the role of peroxisome proliferator-activated receptor gamma (PPARγ) in CIH-induced endothelial dysfunction.
Main Methods:
- Comparative proteomics analysis of rat aortic tissues under CIH and normoxia.
- Bioinformatics analysis to identify differentially expressed proteins and their functions.
- Western blotting and flow cytometry to validate protein expression and cell apoptosis.
Main Results:
- Proteomics identified 3,593 quantified proteins, with 92 upregulated and 468 downregulated in CIH rats.
- Differentially expressed proteins were enriched in energy and lipid metabolism pathways.
- Reduced peroxisome proliferator-activated receptor gamma (PPARγ) expression was observed in CIH-induced endothelial dysfunction, correlating with increased apoptosis. Forced PPARγ expression attenuated apoptosis.
Conclusions:
- Peroxisome proliferator-activated receptor gamma (PPARγ) plays a critical role in endothelial dysfunction associated with chronic intermittent hypoxia (CIH).
- Further research into CIH-related differentially expressed proteins is warranted to understand endothelial dysfunction mechanisms.
