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 inJournal of human hypertension Vol. 32; no. 1; pp. 46 - 53
Main Authors Skrzypkowska, Maria W., Ryba-Stanisławowska, Monika E., Słomiński, Bartosz, Gutknecht, Piotr G., Siebert, Janusz, Myśliwska, Jolanta M.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.01.2018
Nature Publishing Group
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ISSN0950-9240
1476-5527
1476-5527
DOI10.1038/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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ISSN:0950-9240
1476-5527
1476-5527
DOI:10.1038/s41371-017-0020-3