Endothelial Progenitor Cells and NADPH Oxidase Enzyme Activity in the Development of an Aortic Aneurysm

Abstract Introduction: Endothelial progenitor cells (EPCs) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme activity may affect the vessel wall and have a role in development of aortic aneurysms. EPCs originate from hematopoietic stem cells and can be enumerated from peripheral blood samples by flow cytometry. In this study, we aimed to evaluate the relation of EPC number and NADPH oxidase enzyme activity in the development of thoracic aortic aneurysm (TAA). Methods: Patients with TAA (n=30) and healthy individuals without TAA (control, n=10) were included in our study. Characterization and enumeration of EPC from peripheral blood samples were performed by flow cytometry with panels including markers of EPCs (CD34/CD133/CD309/CD146/CD144). Additionally, NADPH oxidase enzyme activity (capacity) was also measured by the dihydrorhodamine 123 (DHR 123) test. Results: The enumeration of EPC with CD34+/CD146+ marker showed that the number of mean EPC/106 cells was increased in the patient group (41.5/106 cells), but not in the control group (20.50/105 cells) (P<0.01). Additionally, patients with TAA presented significantly lower NADPH oxidase activity by DHR assay than healthy controls (mean stimulation index: 60.40± 7.86 and 75.10±5.21, respectively) (P<0.01). Conclusion: Our results showed that the number of EPCs is significantly higher in aortic aneurysm patients and may have a role in disease progression. The crosstalk between NADPH oxidase enzyme capacity and EPC number may be useful as a parameter to explain the clinical progression of TAA.

Endothelial Progenitor Cells and NADPH Oxidase Enzyme Activity in the Development of an Aortic Aneurysm.

INTRODUCTION: Endothelial progenitor cells (EPCs) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme activity may affect the vessel wall and have a role in development of aortic aneurysms. EPCs originate from hematopoietic stem cells and can be enumerated from peripheral blood samples by flow cytometry. In this study, we aimed to evaluate the relation of EPC number and NADPH oxidase enzyme activity in the development of thoracic aortic aneurysm (TAA). METHODS: Patients with TAA (n=30) and healthy individuals without TAA (control, n=10) were included in our study. Characterization and enumeration of EPC from peripheral blood samples were performed by flow cytometry with panels including markers of EPCs (CD34/CD133/CD309/CD146/CD144). Additionally, NADPH oxidase enzyme activity (capacity) was also measured by the dihydrorhodamine 123 (DHR 123) test. RESULTS: The enumeration of EPC with CD34+/CD146+ marker showed that the number of mean EPC/106 cells was increased in the patient group (41.5/106 cells), but not in the control group (20.50/105 cells) (P<0.01). Additionally, patients with TAA presented significantly lower NADPH oxidase activity by DHR assay than healthy controls (mean stimulation index: 60.40± 7.86 and 75.10±5.21, respectively) (P<0.01). CONCLUSION: Our results showed that the number of EPCs is significantly higher in aortic aneurysm patients and may have a role in disease progression. The crosstalk between NADPH oxidase enzyme capacity and EPC number may be useful as a parameter to explain the clinical progression of TAA.

Relationship between thiol, disulphide volume and contrast-induced nephropathy in acute coronary syndrome patients treated with percutaneous coronary intervention.

BACKGROUND: This study aimed to evaluate thiol disulphide volume for the risk of contrast-induced nephropathy (CIN) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). METHODS: A total of 638 patients with ACS were enrolled in the study. CIN was defined as an increase in serum creatinine level of ≥0.5 mg/dL or ≥25% above baseline within 72 h after the procedure. Patients were divided into two groups: patients with and without CIN. Demographics, clinical risk factors, angiographic and laboratory parameters, CIN incidence, thiol, disulphide, and CHA2DS2-VASc score were compared between the two groups. RESULTS: Native thiol, total thiol, and disulphide at baseline were significantly lower in patients who developed CIN compared to those who did not. Also, the CHA2DS2-VASc score was found to be higher in patients with CIN than those without CIN. In receiver operating characteristic analysis showed that at a cutoff of <342.1, the value of native thiol exhibited 82% sensitivity and 80% specificity for detecting CIN. Total thiol< 383.1 calculated on admission had an 80% sensitivity and 80% specificity in predicting CIN. CONCLUSION: Our study suggested that the thiol disulphide volume on admission was independently associated with the development of CIN after PCI in patients with ACS.