Literature DB >> 25707554

Human monocyte subsets exhibit divergent angiotensin I-converting activity.

M Rutkowska-Zapała1, M Suski2, R Szatanek1, M Lenart1, K Węglarczyk1, R Olszanecki2, T Grodzicki3, M Strach3, J Gąsowski3, M Siedlar1.   

Abstract

Immune cells may take part in the renin-angiotensin-aldosterone system (RAAS), which plays a pivotal role in the regulation of vascular tone and blood pressure. The aim of the study was to analyse the expression and activity of angiotensin-converting enzyme type 1 (ACE1) and ACE2 in human monocytes (MO) and their subsets. The highest relative level of ACE1-, as well as ACE2-mRNA expression, was observed in CD14(++)CD16(-) (classical) MO. Moreover, in these cells, mean level of ACE2-mRNA was almost two times higher than that of ACE1-mRNA (11.48 versus 7.073 relative units, respectively). In peripheral blood mononuclear cells (PBMC), MO and classical MO, ACE1 and ACE2 protein expression was stronger compared to other MO subpopulations. The highest level of Ang II generated from Ang I in vitro was observed in classical MO. In this setting, generation of Ang-(1-9) by PBMC and classical MO was higher when compared to the whole MO population (P < 0.05). The generation rate of vasoprotective Ang-(1-7) was comparable in all analysed cell populations. However, in CD14(+)CD16(++) (non-classical) MO, formation of Ang-(1-7) was significantly greater than Ang II (P < 0.001). We suggest that in physiological conditions MO (but also lymphocytes forming the rest of PBMC pool) may be involved in the regulation of vessel wall homeostasis via the RAAS-related mechanisms. Moreover, non-classical MO, which are associated preferentially with the vascular endothelium, express the vasoprotective phenotype.
© 2015 British Society for Immunology.

Entities:  

Keywords:  angiotensin; angiotensin-converting enzymes; monocyte subpopulations; renin-angiotensin-aldosterone system

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Year:  2015        PMID: 25707554      PMCID: PMC4469162          DOI: 10.1111/cei.12612

Source DB:  PubMed          Journal:  Clin Exp Immunol        ISSN: 0009-9104            Impact factor:   4.330


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