{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T17:26:35Z","timestamp":1762017995103,"version":"3.40.5"},"reference-count":0,"publisher":"S. Karger AG","issue":"3","license":[{"start":{"date-parts":[[2016,12,20]],"date-time":"2016-12-20T00:00:00Z","timestamp":1482192000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2016,12,20]],"date-time":"2016-12-20T00:00:00Z","timestamp":1482192000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nephron"],"published-print":{"date-parts":[[2017]]},"abstract":"<b><i>Background:<\/i><\/b> Monocytic products, such as lipoprotein-associated phospholipase A2 (Lp-PLA2), may participate in the development of atherosclerosis. Heterogeneity of monocytes is widely acknowledged. Classical, intermediate, and non-classical subsets can be discerned. Recently, an inflammatory, pro-atherogenic monocyte population could be identified in hemodialysis patients. In this study, we investigated the expression of Lp-PLA2 on leucocytes and different monocyte subpopulations and their possible role in uremia, inflammation, and atherosclerosis. <b><i>Methods:<\/i><\/b> Chronic kidney disease stage 5-D (CKD5-D; <i>n<\/i> = 57), healthy control subjects with hs-C-reactive protein (CRP) levels \u22641 mg\/L (CO-N, <i>n<\/i> = 22) and a control group with inflammatory activation (CRP levels >1 mg\/L, CO-I, <i>n<\/i> = 29) were enrolled in this cross-sectional observation. The CKD5-D cohort was dichotomized into patients with (A+) and without subclinical atherosclerosis (A-) by carotid artery ultrasound measurement. Lp-PLA2 activity was determined in plasma samples, Lp-PLA2 mRNA expression analysis in leucocytes, and sorted monocyte subsets. Effects of Lp-PLA2 overexpression were studied in classical vs. intermediate and non-classical subsets. <b><i>Results:<\/i><\/b> The classical monocytes expressed the highest Lp-PLA2 mRNA levels as compared to other subpopulations. CKD5-D patients revealed significantly higher Lp-PLA2 transcripts, as well as higher Lp-PLA2 plasma activity as compared to healthy and \u201cinflammatory\u201d controls. In vitro data confirmed that uremia significantly contributes to Lp-PLA2 mRNA upregulation. Non-classical monocytes of A+ patients revealed significant higher Lp-PLA2 mRNA compared to A-. <b><i>Conclusion:<\/i><\/b> Uremic environment but not inflammation per se increases plasma Lp-PLA2 activity and upregulates monocytic Lp-PLA2 mRNA expression. The highest Lp-PLA2 levels were found in the classical and not in the inflammatory subsets. Atherosclerosis also contributes to a subset-specific increase in Lp-PLA2 mRNA expression.<\/jats:p>","DOI":"10.1159\/000454778","type":"journal-article","created":{"date-parts":[[2016,12,19]],"date-time":"2016-12-19T22:03:37Z","timestamp":1482185017000},"page":"231-241","source":"Crossref","is-referenced-by-count":6,"title":["Differential Expression of Lipoprotein-Associated Phospholipase A2 in Monocyte Subsets: Impact of Uremia and Atherosclerosis"],"prefix":"10.1159","volume":"135","author":[{"given":"Christof","family":"Ulrich","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7429-381X","authenticated-orcid":false,"given":"Bogusz","family":"Trojanowicz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roman","family":"Fiedler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Felix","family":"Kohler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anna-Franziska","family":"Wolf","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric","family":"Seibert","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthias","family":"Girndt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2016,12,20]]},"container-title":["Nephron"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/454778","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/454778","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/454778","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T17:04:04Z","timestamp":1745427844000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000454778"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2016,12,20]]},"references-count":0,"journal-issue":{"issue":"3","published-online":{"date-parts":[[2017,2,28]]}},"URL":"https:\/\/doi.org\/10.1159\/000454778","archive":["Portico"],"relation":{"is-supplemented-by":[{"id-type":"doi","id":"10.6084\/m9.figshare.4483433","asserted-by":"subject"}]},"ISSN":["1660-8151","2235-3186"],"issn-type":[{"type":"print","value":"1660-8151"},{"type":"electronic","value":"2235-3186"}],"subject":[],"published":{"date-parts":[[2016,12,20]]}}}