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Genome-wide Purification of Extrachromosomal Circular DNA from Eukaryotic Cells
Published on: April 4, 2016
Extracellular DNA affects NO content in human endothelial cells
L V Efremova1, A Yu Alekseeva, M S Konkova
1Medical Genetics Research Center, Russian Academy of Medical Sciences, Russia.
Bulletin of Experimental Biology and Medicine
|November 30, 2010
Summary
Extracellular DNA fragments influence nitric oxide (NO) synthesis in endothelial cells. While healthy DNA boosts NO, DNA from hypertension and atherosclerosis patients reduces it, linked to CG-rich sequences.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Biochemistry
Background:
- Extracellular DNA (eDNA) is released into circulation via apoptosis and synthesis.
- Nitric oxide (NO) is a critical regulator of vascular tone.
- The impact of eDNA on NO synthesis remains largely unexplored.
Purpose of the Study:
- To investigate the in vitro effect of eDNA on NO synthesis in human umbilical vein endothelial cells (HUVECs).
- To determine if DNA sequence and concentration influence NO production.
- To compare the effects of eDNA from healthy individuals and patients with cardiovascular diseases.
Main Methods:
- Utilized HUVEC cultures to assess NO synthesis.
- Employed artificial DNA probes and eDNA samples from healthy and diseased individuals.
- Quantified NO using a cell-penetrating NO-specific fluorescent probe (CuFL).
Main Results:
- Human genome DNA fragments modulated NO levels in HUVECs, dependent on sequence and concentration.
- Low concentrations (5 ng/ml) of artificial and healthy eDNA increased NO by up to 4-fold.
- Cytosine-guanine (CG)-rich sequences acted as potent NO inducers.
- eDNA from hypertensive and atherosclerotic patients reduced NO by 1.3-28 times, correlating with CG content.
Conclusions:
- Extracellular DNA significantly impacts endothelial NO synthesis.
- The sequence composition, particularly CG-rich regions, and concentration of eDNA are key modulators.
- Dysfunctional eDNA in cardiovascular diseases may contribute to impaired NO bioavailability.
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