Plasma levels of E-selectin are associated with retinopathy in sickle cell disease.
E-selectin
endothelium markers
sickle cell disease
sickle cell vasculopathy
Journal
European journal of haematology
ISSN: 1600-0609
Titre abrégé: Eur J Haematol
Pays: England
ID NLM: 8703985
Informations de publication
Date de publication:
Mar 2023
Mar 2023
Historique:
revised:
11
11
2022
received:
07
08
2022
accepted:
14
11
2022
pubmed:
22
11
2022
medline:
4
2
2023
entrez:
21
11
2022
Statut:
ppublish
Résumé
The vascular endothelium is markedly disrupted in sickle cell disease (SCD) and is the converging cascade of the complex pathophysiologic processes linked to sickle cell vasculopathy. Circulating endothelial activation and/or apoptotic markers may reflect this endothelial activation/damage that contributes to the pathophysiology of the SCD vascular complications. Plasmatic levels of circulating endothelial cells (CECs), E-selectin, progenitor's endothelial cells (EPCs), and circulating extracellular vesicles (EVs) were evaluated in 50 SCD patients, 16 with vasculopathy. The association between these markers and the occurrence of disease-related microvascular injuries of the eye (retinopathy), kidney (nephropathy), and skin (chronic active ulcers) was explored. Among the endothelial activation markers studied, only higher plasma levels of E-selectin were found in SCD patients with vasculopathy (p = .015). Increased E-selectin levels were associated with retinopathy (p < .001) but not with nephropathy or leg ulcers. All patients, at steady state, with or without vasculopathy, did not display a high count of CEC and EPC, markers of endothelial injury and repair. We did not show any significant differences in EVs levels between vasculopathy and not vasculopathy SCD patients. Further studies will be required to determine whether the E-selectin could be used as an early biomarker of retinopathy sickle cell development.
Sections du résumé
BACKGROUND
BACKGROUND
The vascular endothelium is markedly disrupted in sickle cell disease (SCD) and is the converging cascade of the complex pathophysiologic processes linked to sickle cell vasculopathy. Circulating endothelial activation and/or apoptotic markers may reflect this endothelial activation/damage that contributes to the pathophysiology of the SCD vascular complications.
METHODS
METHODS
Plasmatic levels of circulating endothelial cells (CECs), E-selectin, progenitor's endothelial cells (EPCs), and circulating extracellular vesicles (EVs) were evaluated in 50 SCD patients, 16 with vasculopathy. The association between these markers and the occurrence of disease-related microvascular injuries of the eye (retinopathy), kidney (nephropathy), and skin (chronic active ulcers) was explored.
RESULTS
RESULTS
Among the endothelial activation markers studied, only higher plasma levels of E-selectin were found in SCD patients with vasculopathy (p = .015). Increased E-selectin levels were associated with retinopathy (p < .001) but not with nephropathy or leg ulcers. All patients, at steady state, with or without vasculopathy, did not display a high count of CEC and EPC, markers of endothelial injury and repair. We did not show any significant differences in EVs levels between vasculopathy and not vasculopathy SCD patients.
CONCLUSIONS
CONCLUSIONS
Further studies will be required to determine whether the E-selectin could be used as an early biomarker of retinopathy sickle cell development.
Identifiants
pubmed: 36409296
doi: 10.1111/ejh.13902
pmc: PMC10100354
doi:
Substances chimiques
E-Selectin
0
SELE protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
271-279Subventions
Organisme : AORC 2012-13 (Appel d'Offres de Recherche Clinique).
Informations de copyright
© 2022 The Authors. European Journal of Haematology published by John Wiley & Sons Ltd.
Références
Blood Adv. 2020 Apr 14;4(7):1501-1511
pubmed: 32289161
N Engl J Med. 1994 Jun 9;330(23):1639-44
pubmed: 7993409
Am J Hematol. 2010 Jul;85(7):532-5
pubmed: 20575034
J Clin Invest. 1997 Apr 15;99(8):1809-13
pubmed: 9109423
N Engl J Med. 2017 Feb 2;376(5):429-439
pubmed: 27959701
Am J Respir Crit Care Med. 2003 Jul 1;168(1):63-9
pubmed: 12626350
Thromb Haemost. 2005 Feb;93(2):228-35
pubmed: 15711737
J Clin Invest. 2017 Mar 1;127(3):750-760
pubmed: 28248201
Blood Coagul Fibrinolysis. 2005 Apr;16(3):209-14
pubmed: 15795541
Curr Stem Cell Res Ther. 2010 Dec;5(4):294-302
pubmed: 20528750
Nat Rev Dis Primers. 2018 Mar 15;4:18010
pubmed: 29542687
Blood. 2016 Feb 18;127(7):810-9
pubmed: 26758919
Microcirculation. 2004 Mar;11(2):167-77
pubmed: 15280090
J Thromb Haemost. 2012 Mar;10(3):437-46
pubmed: 22212198
J Cardiovasc Transl Res. 2011 Dec;4(6):811-22
pubmed: 21786187
Blood. 2020 Jul 9;136(2):247-256
pubmed: 32285120
Clin Exp Med. 2008 Sep;8(3):159-64
pubmed: 18791689
Br J Ophthalmol. 2002 Apr;86(4):363-5
pubmed: 11914197
Graefes Arch Clin Exp Ophthalmol. 2017 Jan;255(1):25-30
pubmed: 27377657
Circulation. 2003 Jan 21;107(2):271-8
pubmed: 12538427
Br J Haematol. 2005 Sep;130(6):943-53
pubmed: 16156864
J Diabetes Complications. 2006 May-Jun;20(3):188-95
pubmed: 16632240
Haematologica. 2011 Jan;96(1):1-5
pubmed: 21193426
N Engl J Med. 2017 Apr 20;376(16):1561-1573
pubmed: 28423290
Br J Haematol. 2015 Nov;171(4):615-24
pubmed: 26205481
Br J Ophthalmol. 2002 Jun;86(6):684-90
pubmed: 12034693
Hematology Am Soc Hematol Educ Program. 2008;:177-85
pubmed: 19074078
Br J Haematol. 2016 Jul;174(1):16-29
pubmed: 27136195
Pediatr Crit Care Med. 2008 Mar;9(2):159-68
pubmed: 18477929
J Lab Clin Med. 1997 May;129(5):507-16
pubmed: 9142047
J Cell Mol Med. 2009 Mar;13(3):454-71
pubmed: 19379144
Blood Rev. 2007 Mar;21(2):99-111
pubmed: 16987572
Blood. 2013 Dec 5;122(24):3892-8
pubmed: 24052549
N Engl J Med. 1980 May 1;302(18):992-5
pubmed: 7366623
Blood. 2015 Apr 23;125(17):2656-64
pubmed: 25733584
Blood. 2003 Oct 1;102(7):2678-83
pubmed: 12805058
Am J Hematol. 2009 Sep;84(9):618-25
pubmed: 19610078
Haematologica. 2015 Jul;100(7):870-80
pubmed: 25934765
Int Urol Nephrol. 2018 Jun;50(6):1075-1083
pubmed: 29383580
Platelets. 2013;24(8):605-14
pubmed: 23249216
Blood Cells Mol Dis. 2009 Jul-Aug;43(1):63-7
pubmed: 19356955
Haematologica. 2009 Nov;94(11):1513-9
pubmed: 19815831
PLoS One. 2014 Jan 24;9(1):e87243
pubmed: 24475257
Lancet. 2013 Jan 12;381(9861):142-51
pubmed: 23103089
N Engl J Med. 2008 Nov 20;359(21):2254-65
pubmed: 19020327
Blood. 2014 Jun 12;123(24):3720-6
pubmed: 24764565
Blood Cells Mol Dis. 2015 Jan;54(1):33-7
pubmed: 25172543
Front Immunol. 2020 Mar 13;11:454
pubmed: 32231672
Am J Hematol. 2005 May;79(1):17-25
pubmed: 15849770
J Extracell Vesicles. 2018 Nov 23;7(1):1535750
pubmed: 30637094
J Thromb Thrombolysis. 2014;38(2):167-75
pubmed: 24254379
Biomark Med. 2018 Feb;12(2):161-175
pubmed: 29327597
Am J Ophthalmol. 1971 Mar;71(3):649-65
pubmed: 5546311
Semin Thromb Hemost. 2011 Apr;37(3):226-36
pubmed: 21455857
Thromb Haemost. 1999 Nov;82(5):1433-6
pubmed: 10595633
Nat Med. 2009 Apr;15(4):384-91
pubmed: 19305412
Lancet. 2010 Dec 11;376(9757):2018-31
pubmed: 21131035
Circulation. 2013 Mar 26;127(12):1317-29
pubmed: 23446829
Nat Rev Drug Discov. 2019 Feb;18(2):139-158
pubmed: 30514970
Eur J Haematol. 2023 Mar;110(3):271-279
pubmed: 36409296
Nature. 1993 Apr 29;362(6423):801-9
pubmed: 8479518
Lancet. 2010 Jul 10;376(9735):124-36
pubmed: 20580421