title: Human monocyte subsets exhibit divergent angiotensin I-converting activity.
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.
authors.affiliation: Department of Clinical Immunology, Polish-American Institute of Pediatrics.
authors.forename: M
authors.initials: M
authors.lastname: Rutkowska-Zapała
authors.affiliation: Department of Pharmacology.
authors.forename: M
authors.initials: M
authors.lastname: Suski
authors.affiliation: Department of Clinical Immunology, Polish-American Institute of Pediatrics.
authors.forename: R
authors.initials: R
authors.lastname: Szatanek
authors.affiliation: Department of Clinical Immunology, Polish-American Institute of Pediatrics.
authors.forename: M
authors.initials: M
authors.lastname: Lenart
authors.affiliation: Department of Clinical Immunology, Polish-American Institute of Pediatrics.
authors.forename: K
authors.initials: K
authors.lastname: Węglarczyk
authors.affiliation: Department of Pharmacology.
authors.forename: R
authors.initials: R
authors.lastname: Olszanecki
authors.affiliation: Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland.
authors.forename: T
authors.initials: T
authors.lastname: Grodzicki
authors.affiliation: Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland.
authors.forename: M
authors.initials: M
authors.lastname: Strach
authors.affiliation: Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Gąsowski
authors.affiliation: Department of Clinical Immunology, Polish-American Institute of Pediatrics.
authors.forename: M
authors.initials: M
authors.lastname: Siedlar
mesh_terms: D000085962:Angiotensin-Converting Enzyme 2; D058851:GPI-Linked Proteins / Q000276:immunology; D064368:Healthy Volunteers; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D009000:Monocytes / Q000201:enzymology* / Q000276:immunology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D017452:Receptors, IgG / Q000276:immunology; D012084:Renin-Angiotensin System / Q000276:immunology
chemical_list: C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger; D017452:Receptors, IgG; D007703:Peptidyl-Dipeptidase A; C000705307:ACE2 protein, human; D000085962:Angiotensin-Converting Enzyme 2
keywords: angiotensin; angiotensin-converting enzymes; monocyte subpopulations; renin-angiotensin-aldosterone system