Plasma glycocalyx pattern: a mirror of endothelial damage in chronic kidney disease.
chronic kidney disease
decorin
endothelial dysfunction
monocyte adhesion
perlecan
Journal
Clinical kidney journal
ISSN: 2048-8505
Titre abrégé: Clin Kidney J
Pays: England
ID NLM: 101579321
Informations de publication
Date de publication:
Aug 2023
Aug 2023
Historique:
received:
30
06
2022
medline:
2
8
2023
pubmed:
2
8
2023
entrez:
2
8
2023
Statut:
epublish
Résumé
Endothelial damage and cardiovascular disease complicate chronic kidney disease (CKD). The increased atherogenicity observed in patients with CKD can be linked to microinflammation and endothelial damage. Circulating endothelial glycocalyx degradation products, such as perlecan and decorin, tend to be elevated in CKD. We aimed to explore the association between the plasma perlecan and decorin levels and this pro-inflammatory and atherogenic state by studying monocyte subpopulations and intracellular adhesion molecule (ICAM)-1 expression in patients with CKD. We studied 17 healthy controls, 23 patients with advanced CKD, 25 patients on haemodialysis, 23 patients on peritoneal dialysis and 20 patients who underwent kidney transplantation. Perlecan and decorin levels were evaluated using enzyme-linked immunosorbent assays, and the monocyte phenotype was analysed using direct immunofluorescence and flow cytometry. The plasma perlecan levels were higher in patients with CKD than in the healthy controls. These levels were associated with a higher prevalence of ICAM-1+ monocytes. Conversely, patients with advanced CKD (pre-dialysis) had higher plasma decorin levels, which were associated with a reduced ICAM-1 expression per monocyte. Elevated perlecan levels in CKD may be associated with a higher prevalence of ICAM-1+ monocytes and a pro-inflammatory phenotype. Elevated decorin levels may act as a negative regulator of ICAM-1 expression in monocytes. Therefore, perlecan and decorin may be related to inflammation and monocyte activation in CKD and may act as potential markers of endothelial damage.
Sections du résumé
Background
UNASSIGNED
Endothelial damage and cardiovascular disease complicate chronic kidney disease (CKD). The increased atherogenicity observed in patients with CKD can be linked to microinflammation and endothelial damage. Circulating endothelial glycocalyx degradation products, such as perlecan and decorin, tend to be elevated in CKD. We aimed to explore the association between the plasma perlecan and decorin levels and this pro-inflammatory and atherogenic state by studying monocyte subpopulations and intracellular adhesion molecule (ICAM)-1 expression in patients with CKD.
Methods
UNASSIGNED
We studied 17 healthy controls, 23 patients with advanced CKD, 25 patients on haemodialysis, 23 patients on peritoneal dialysis and 20 patients who underwent kidney transplantation. Perlecan and decorin levels were evaluated using enzyme-linked immunosorbent assays, and the monocyte phenotype was analysed using direct immunofluorescence and flow cytometry.
Results
UNASSIGNED
The plasma perlecan levels were higher in patients with CKD than in the healthy controls. These levels were associated with a higher prevalence of ICAM-1+ monocytes. Conversely, patients with advanced CKD (pre-dialysis) had higher plasma decorin levels, which were associated with a reduced ICAM-1 expression per monocyte.
Conclusions
UNASSIGNED
Elevated perlecan levels in CKD may be associated with a higher prevalence of ICAM-1+ monocytes and a pro-inflammatory phenotype. Elevated decorin levels may act as a negative regulator of ICAM-1 expression in monocytes. Therefore, perlecan and decorin may be related to inflammation and monocyte activation in CKD and may act as potential markers of endothelial damage.
Identifiants
pubmed: 37529650
doi: 10.1093/ckj/sfad051
pii: sfad051
pmc: PMC10387401
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1278-1287Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the ERA.
Déclaration de conflit d'intérêts
None declared.
Références
Antioxidants (Basel). 2021 Jul 20;10(7):
pubmed: 34356387
Infect Immun. 2005 Oct;73(10):6493-8
pubmed: 16177322
Front Med (Lausanne). 2021 Sep 27;8:705159
pubmed: 34646838
Kidney Blood Press Res. 2021;46(5):581-587
pubmed: 34320503
J Intern Med. 2016 Jul;280(1):97-113
pubmed: 26749537
Atherosclerosis. 2014 Jun;234(2):335-43
pubmed: 24727235
Annu Rev Biomed Eng. 2007;9:121-67
pubmed: 17373886
Circ Res. 2018 Sep 14;123(7):849-867
pubmed: 30355080
Br J Pharmacol. 2017 Jun;174(12):1591-1619
pubmed: 27187006
Matrix Biol. 2015 Apr;43:15-26
pubmed: 25661523
Crit Care Clin. 2020 Apr;36(2):217-232
pubmed: 32172810
Am J Pathol. 2020 Apr;190(4):791-798
pubmed: 32035882
Clin Kidney J. 2022 Oct 19;16(2):384-393
pubmed: 36755834
Pflugers Arch. 2007 Jun;454(3):345-59
pubmed: 17256154
Physiol Res. 2019 Oct 25;68(5):775-783
pubmed: 31424258
J Intensive Care Med. 2021 Nov;36(11):1286-1295
pubmed: 32799720
Front Biosci (Landmark Ed). 2009 Jun 01;14(13):4932-49
pubmed: 19482596
Clin Chim Acta. 1996 Nov 29;255(2):119-32
pubmed: 8937755
Arterioscler Thromb Vasc Biol. 2004 Dec;24(12):2391-6
pubmed: 15472131
PLoS One. 2012;7(9):e44076
pubmed: 23028487
Adv Drug Deliv Rev. 2022 May;184:114195
pubmed: 35292326
Int J Environ Res Public Health. 2021 Jul 29;18(15):
pubmed: 34360333
J Am Soc Nephrol. 2019 May;30(5):726-736
pubmed: 31000567
J Biol Chem. 2021 Jan-Jun;296:100520
pubmed: 33684447
Contrib Nephrol. 2011;171:57-61
pubmed: 21625090
Biochim Biophys Acta Gen Subj. 2019 May;1863(5):839-848
pubmed: 30794825
Am J Kidney Dis. 2005 Feb;45(2):353-9
pubmed: 15685514
J Am Soc Nephrol. 2017 Apr;28(4):1278-1285
pubmed: 27799487
Toxins (Basel). 2020 Jun 20;12(6):
pubmed: 32575762
FASEB J. 2001 Mar;15(3):559-61
pubmed: 11259366
Front Cardiovasc Med. 2022 Jul 01;9:952022
pubmed: 35845081
Nephron. 2019;143(4):234-242
pubmed: 31514183
Nat Rev Nephrol. 2019 Feb;15(2):87-108
pubmed: 30607032
Toxins (Basel). 2018 Sep 23;10(10):
pubmed: 30249039
Front Cell Dev Biol. 2021 Sep 21;9:733015
pubmed: 34621749
Am J Pathol. 2020 Apr;190(4):768-780
pubmed: 32035885
Crit Care. 2019 Jan 17;23(1):16
pubmed: 30654825
Clin Kidney J. 2019 Apr 23;12(5):611-619
pubmed: 31583086
BMC Nephrol. 2021 Jan 10;22(1):21
pubmed: 33423673
Stroke. 2019 Oct;50(10):2948-2951
pubmed: 31409270
Front Cell Dev Biol. 2020 Mar 20;8:185
pubmed: 32266265
Braz J Med Biol Res. 2019 Nov 25;52(12):e8658
pubmed: 31778438
Front Cell Dev Biol. 2021 Apr 01;9:623582
pubmed: 33869173
Am J Kidney Dis. 2002 Feb;39(2):266-73
pubmed: 11840366
PLoS One. 2014 Oct 08;9(10):e109596
pubmed: 25295599
J Immunol. 2011 Feb 1;186(3):1809-15
pubmed: 21191073
Matrix Biol. 2021 Jan;95:1-14
pubmed: 33065248
J Am Soc Nephrol. 2012 Nov;23(11):1900-8
pubmed: 23085635
Atherosclerosis. 2014 Mar;233(1):113-21
pubmed: 24529131
Free Radic Biol Med. 2000 May 1;28(9):1379-86
pubmed: 10924857
J Leukoc Biol. 2019 Jan;105(1):81-92
pubmed: 30376187
Curr Opin Nephrol Hypertens. 2022 May 1;31(3):235-243
pubmed: 35142744