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Updated: May 2, 2026

Isolation of Endothelial Progenitor Cells from Human Umbilical Cord Blood
Published on: September 14, 2017
Circulating progenitor cells in hypertensive patients with different degrees of cardiovascular involvement
G Mandraffino1, E Imbalzano1, M A Sardo1
1Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Insights
Hypertension impacts proangiogenic hematopoietic cells (PHCs) differently based on cardiovascular involvement. Arterial stiffening increases PHCs with oxidative stress, while left ventricular hypertrophy reduces them.
Area of Science:
- Cardiovascular Biology
- Hematology
- Oxidative Stress Research
Background:
- Hypertension is linked to cardiovascular damage and altered circulating cell populations.
- Proangiogenic hematopoietic cells (PHCs) play a role in vascular health, but their behavior in different hypertension stages is unclear.
- The redox system and microRNA expression within PHCs may be affected by hypertensive cardiovascular involvement.
Purpose of the Study:
- To investigate the association between hypertension-related cardiovascular involvement (arterial stiffening vs. left ventricular hypertrophy) and PHC numbers, phenotypes, and redox status.
- To evaluate microRNA (miRs) 221/222 expression in CD34+ cells and its relationship with cell number, reactive oxygen species (ROS), and key redox enzymes.
- To compare these parameters between isolated arterial stiffening (AS) hypertensives and those with left ventricular hypertrophy (LVH).
Main Methods:
- Isolation of PHCs from hypertensive patients and controls using flow cytometry.
- Analysis of CD34+ cell expression of miRs 221/222, ROS levels, and redox enzymes (MnSOD, CAT, GPx-1, NOX2).
- Comparison of PHC numbers and redox system components across different hypertensive subgroups (AS, LVH) and controls.
Main Results:
- PHCs were elevated in hypertensives compared to controls but lower in LVH than in AS hypertensives.
- In AS hypertensives, CD34+ cells showed overexpression of NOX2, MnSOD, CAT, and GPx-1, with increased ROS and miRs associated with cell number.
- In LVH, an imbalanced redox system (high MnSOD, low CAT/GPx-1) was observed, with higher ROS and miRs inversely associated with cell number.
Conclusions:
- In AS hypertensives, a balanced redox system may support increased PHCs.
- In hypertensives with more advanced lesions (LVH), redox imbalance likely leads to increased oxidative stress and reduced PHCs.
- These findings highlight distinct PHC responses and redox alterations in different stages of hypertensive cardiovascular involvement.
Abstract:
We investigated whether different degrees of hypertension-related cardiovascular involvement are associated with changes in circulating proangiogenic hematopoietic cell (PHC) numbers and/or phenotypes and/or in the PHC redox system in hypertensive individuals with isolated arterial stiffening (AS) hypertensives or with both carotid intima-media thickening and left ventricular hypertrophy (LVH) hypertensives. We also evaluated microRNA (miRs) 221 and 222 (miRs221/222) expression in CD34+ cells, the relationship between these miRs and cell number and reactive oxygen species (ROS) levels, and the expression of manganese superoxide dismutase (MnSOD), catalase (CAT) glutathione peroxidase type-1 (GPx-1) and gp91phox-containing nicotinamide-adenine-dinucleotide-phosphate-oxidase (NOX2). Proangiogenic hematopoietic cells (PHCs) from hypertensive patients and controls were isolated by flow cytometry. PHCs were higher in hypertensives than in controls but were lower in LVH than in AS hypertensives. In CD34+ cells from AS hypertensives, NOX2, MnSOD, CAT and GPx-1 were overexpressed; ROS, miRs and NOX2 were also increased and were associated with cell number. In LVH, we found an imbalance in the cell redox system; MnSOD showed the highest values, whereas CAT and GPx-1 were lower than in AS hypertensives. Intracellular ROS, miRs and NOX2 were higher and inversely associated with cell number. In AS hypertensives, the redox balance may sustain the increase in PHCs; by contrast, in hypertensives with more advanced lesions, redox imbalance may result in increased oxidative stress and cell reduction.
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