Matches in SemOpenAlex for { <https://semopenalex.org/work/W2987751593> ?p ?o ?g. }
- W2987751593 endingPage "515" @default.
- W2987751593 startingPage "502" @default.
- W2987751593 abstract "Dysfunctional high-density lipoprotein (d-HDL) in chronic kidney disease is known to have a change in composition towards an endothelial-damaging phenotype, amongst others, via the accumulation of symmetric dimethylarginine. The endothelial glycocalyx, a carbohydrate-rich layer lining the endothelial luminal surface, is a first line defense against vascular diseases including atherosclerosis. Here we conducted a translational, cross-sectional study to determine the role of symmetric dimethylarginine in d-HDL as a mediator of glycocalyx damage. Using confocal and atomic force microscopy, intact HDL from healthy donors was found to maintain the glycocalyx while isolated HDL from hemodialysis patients and exogenous symmetric dimethylarginine caused significant damage to the glycocalyx in endothelial cells in vitro in a dose-dependent manner. Symmetric dimethylarginine triggered glycocalyx deterioration via molecular pathways mediated by toll-like-receptor 2 and matrix metalloprotease-9. Corresponding intravital microscopy revealed that exogenous symmetric dimethylarginine and d-HDL from hemodialysis patients caused glycocalyx breakdown, which subsequently contributed to alterations in leukocyte rolling. Biologically effective HDL, which estimates the functionality of HDL, was calculated from circulating HDL-cholesterol and symmetric dimethylarginine, as described in the literature. Biologically effective HDL was the only parameter that could independently predict glycocalyx damage in vivo. Thus, our data suggest that symmetric dimethylarginine in d-HDL mediates glycocalyx breakdown in chronic kidney disease. Dysfunctional high-density lipoprotein (d-HDL) in chronic kidney disease is known to have a change in composition towards an endothelial-damaging phenotype, amongst others, via the accumulation of symmetric dimethylarginine. The endothelial glycocalyx, a carbohydrate-rich layer lining the endothelial luminal surface, is a first line defense against vascular diseases including atherosclerosis. Here we conducted a translational, cross-sectional study to determine the role of symmetric dimethylarginine in d-HDL as a mediator of glycocalyx damage. Using confocal and atomic force microscopy, intact HDL from healthy donors was found to maintain the glycocalyx while isolated HDL from hemodialysis patients and exogenous symmetric dimethylarginine caused significant damage to the glycocalyx in endothelial cells in vitro in a dose-dependent manner. Symmetric dimethylarginine triggered glycocalyx deterioration via molecular pathways mediated by toll-like-receptor 2 and matrix metalloprotease-9. Corresponding intravital microscopy revealed that exogenous symmetric dimethylarginine and d-HDL from hemodialysis patients caused glycocalyx breakdown, which subsequently contributed to alterations in leukocyte rolling. Biologically effective HDL, which estimates the functionality of HDL, was calculated from circulating HDL-cholesterol and symmetric dimethylarginine, as described in the literature. Biologically effective HDL was the only parameter that could independently predict glycocalyx damage in vivo. Thus, our data suggest that symmetric dimethylarginine in d-HDL mediates glycocalyx breakdown in chronic kidney disease. Dysfunctional HDL takes its Toll on the endothelial glycocalyxKidney InternationalVol. 97Issue 3PreviewPatients with end-stage renal disease have a high risk of dying from cardiovascular disease that cannot be explained solely by traditional cardiovascular disease risk factors. Hesse et al. suggest that dysfunctional high-density lipoprotein cholesterol generated in patients with end-stage renal disease causes endothelial glycocalyx degradation. Glycocalyx degradation may represent one of the earliest insults leading to atheroma formation, and so this work suggests a novel link between renal failure and cardiovascular disease. Full-Text PDF" @default.
- W2987751593 created "2019-11-22" @default.
- W2987751593 creator A5006539980 @default.
- W2987751593 creator A5012660143 @default.
- W2987751593 creator A5019459931 @default.
- W2987751593 creator A5030129034 @default.
- W2987751593 creator A5033699907 @default.
- W2987751593 creator A5035295431 @default.
- W2987751593 creator A5040277117 @default.
- W2987751593 creator A5059453823 @default.
- W2987751593 creator A5068650860 @default.
- W2987751593 creator A5071509240 @default.
- W2987751593 creator A5084969405 @default.
- W2987751593 creator A5088151341 @default.
- W2987751593 date "2020-03-01" @default.
- W2987751593 modified "2023-09-30" @default.
- W2987751593 title "Symmetric dimethylarginine in dysfunctional high-density lipoprotein mediates endothelial glycocalyx breakdown in chronic kidney disease" @default.
- W2987751593 cites W1993912121 @default.
- W2987751593 cites W1995983036 @default.
- W2987751593 cites W1998790528 @default.
- W2987751593 cites W2007699321 @default.
- W2987751593 cites W2016040116 @default.
- W2987751593 cites W2017295052 @default.
- W2987751593 cites W2017585564 @default.
- W2987751593 cites W2017754180 @default.
- W2987751593 cites W2020732104 @default.
- W2987751593 cites W2024184035 @default.
- W2987751593 cites W2032576629 @default.
- W2987751593 cites W2035665444 @default.
- W2987751593 cites W2044642923 @default.
- W2987751593 cites W2062340475 @default.
- W2987751593 cites W2072845370 @default.
- W2987751593 cites W2075603768 @default.
- W2987751593 cites W2091408336 @default.
- W2987751593 cites W2101773230 @default.
- W2987751593 cites W2106422918 @default.
- W2987751593 cites W2111247242 @default.
- W2987751593 cites W2111766323 @default.
- W2987751593 cites W2111879266 @default.
- W2987751593 cites W2115220026 @default.
- W2987751593 cites W2124704048 @default.
- W2987751593 cites W2125342621 @default.
- W2987751593 cites W2125455679 @default.
- W2987751593 cites W2132478456 @default.
- W2987751593 cites W2132612851 @default.
- W2987751593 cites W2133930237 @default.
- W2987751593 cites W2135427169 @default.
- W2987751593 cites W2136057035 @default.
- W2987751593 cites W2139976637 @default.
- W2987751593 cites W2143221056 @default.
- W2987751593 cites W2143914224 @default.
- W2987751593 cites W2152252241 @default.
- W2987751593 cites W2152678130 @default.
- W2987751593 cites W2153870838 @default.
- W2987751593 cites W2156414024 @default.
- W2987751593 cites W2157773442 @default.
- W2987751593 cites W2158057499 @default.
- W2987751593 cites W2158214252 @default.
- W2987751593 cites W2165758797 @default.
- W2987751593 cites W2166283593 @default.
- W2987751593 cites W2293575722 @default.
- W2987751593 cites W2324841714 @default.
- W2987751593 cites W2327067198 @default.
- W2987751593 cites W2480349329 @default.
- W2987751593 cites W2561478950 @default.
- W2987751593 cites W2587131188 @default.
- W2987751593 cites W2590046353 @default.
- W2987751593 cites W2604704258 @default.
- W2987751593 cites W2747816469 @default.
- W2987751593 cites W2767573195 @default.
- W2987751593 cites W2768132763 @default.
- W2987751593 cites W2802890170 @default.
- W2987751593 cites W2887314695 @default.
- W2987751593 cites W2897015753 @default.
- W2987751593 doi "https://doi.org/10.1016/j.kint.2019.10.017" @default.
- W2987751593 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32008804" @default.
- W2987751593 hasPublicationYear "2020" @default.
- W2987751593 type Work @default.
- W2987751593 sameAs 2987751593 @default.
- W2987751593 citedByCount "16" @default.
- W2987751593 countsByYear W29877515932020 @default.
- W2987751593 countsByYear W29877515932021 @default.
- W2987751593 countsByYear W29877515932022 @default.
- W2987751593 countsByYear W29877515932023 @default.
- W2987751593 crossrefType "journal-article" @default.
- W2987751593 hasAuthorship W2987751593A5006539980 @default.
- W2987751593 hasAuthorship W2987751593A5012660143 @default.
- W2987751593 hasAuthorship W2987751593A5019459931 @default.
- W2987751593 hasAuthorship W2987751593A5030129034 @default.
- W2987751593 hasAuthorship W2987751593A5033699907 @default.
- W2987751593 hasAuthorship W2987751593A5035295431 @default.
- W2987751593 hasAuthorship W2987751593A5040277117 @default.
- W2987751593 hasAuthorship W2987751593A5059453823 @default.
- W2987751593 hasAuthorship W2987751593A5068650860 @default.
- W2987751593 hasAuthorship W2987751593A5071509240 @default.
- W2987751593 hasAuthorship W2987751593A5084969405 @default.
- W2987751593 hasAuthorship W2987751593A5088151341 @default.
- W2987751593 hasConcept C126322002 @default.