Association of circulating progenitor cells with angiotensin II in newly diagnosed hypertensive patients
Populations of CD34− and VEGFR2-expressing cells are responsible for regeneration of damaged endothelium and vascular remodelling. As their quantity and activity changes during cardiovascular diseases, they are potentially useful markers of cardiovascular health. The aim of our study was to investig...
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Published in | Journal of human hypertension Vol. 32; no. 1; pp. 46 - 53 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.01.2018
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 0950-9240 1476-5527 1476-5527 |
DOI | 10.1038/s41371-017-0020-3 |
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Summary: | Populations of CD34− and VEGFR2-expressing cells are responsible for regeneration of damaged endothelium and vascular remodelling. As their quantity and activity changes during cardiovascular diseases, they are potentially useful markers of cardiovascular health. The aim of our study was to investigate changes of various CD34+ and CD34+ VEGFR2+ populations in subjects with newly recognised hypertension and to evaluate whether observed alterations are influenced by clinical parameters and angiotensin II. Circulating CD34+ and CD34+ VEGFR2+ cells were analysed in peripheral blood samples by flow cytometry. Serum levels of angiotensin II were determined using immunoenzymatic assay. We discovered increased proportions of various CD34+ populations and CD34+ VEGFR2+ c-Kit+ cells in newly diagnosed patients. CD34+ cells seem to be influenced by angiotensin II, but we did not observe comparable results when populations co-expressing VEGFR2 were analysed. The quantity of CD34+ VEGFR2+ cells in patients with newly recognised primary hypertension ought to be determined by other factors. Increased proportions of CD34+ progenitors in blood could comprise compensatory mechanism for increased endothelial damage in hypertension. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 0950-9240 1476-5527 1476-5527 |
DOI: | 10.1038/s41371-017-0020-3 |