Association of serum levels of antibodies against ALDOA and FH4 with transient ischemic attack and cerebral infarction.
ALDOA
Antibody biomarker
Cerebral infarction
FH
Transient ischemic attack
Journal
BMC neurology
ISSN: 1471-2377
Titre abrégé: BMC Neurol
Pays: England
ID NLM: 100968555
Informations de publication
Date de publication:
09 Jul 2021
09 Jul 2021
Historique:
received:
18
03
2020
accepted:
28
06
2021
entrez:
10
7
2021
pubmed:
11
7
2021
medline:
20
7
2021
Statut:
epublish
Résumé
Ischemic stroke, including transient ischemic attack (TIA) and acute-phase cerebral infarction (aCI), is a serious health problem in the aging society. Thus, this study aimed to identify TIA and aCI biomarkers. In 19 patients with TIA, candidate antigens recognized by serum IgG autoantibodies were screened using a human aortic endothelial cell cDNA library. Through amplified luminescent proximity homogeneous assay-linked immunosorbent assay (AlphaLISA), serum antibody levels against the candidate antigens were examined in healthy donor (HD), TIA, and aCI cohorts (n = 285, 92, and 529). The plasma antibody levels in the Japan Public Health Center-based Prospective Cohort Study (1991-1993) were also examined. The candidate antigens were aldolase A (ALDOA) and fumarate hydratase (FH). In AlphaLISA, patients with TIA or aCI had higher anti-ALDOA antibody (ALDOA-Ab) and anti-FH antibody (FH-Ab) levels than the HDs (P < 0.05). In a multivariate logistic regression analysis, the ALDOA-Ab (odds ratio [OR]: 2.46, P = 0.0050) and FH-Ab (OR: 2.49, P = 0.0037) levels were independent predictors of TIA. According to the case-control study, the ALDOA-Ab (OR: 2.50, P < 0.01) and FH-Ab (OR: 2.60, P < 0.01) levels were associated with aCI risk. In a correlation analysis, both ALDOA-Abs and FH-Abs were well associated with hypertension, coronary heart disease, and habitual smoking. These antibody levels also correlated well with maximum intima-media thickness, which reflects atherosclerotic stenosis. ALDOA-Abs and FH-Abs can be novel potential biomarkers for predicting atherosclerotic TIA and aCI.
Sections du résumé
BACKGROUND
BACKGROUND
Ischemic stroke, including transient ischemic attack (TIA) and acute-phase cerebral infarction (aCI), is a serious health problem in the aging society. Thus, this study aimed to identify TIA and aCI biomarkers.
METHODS
METHODS
In 19 patients with TIA, candidate antigens recognized by serum IgG autoantibodies were screened using a human aortic endothelial cell cDNA library. Through amplified luminescent proximity homogeneous assay-linked immunosorbent assay (AlphaLISA), serum antibody levels against the candidate antigens were examined in healthy donor (HD), TIA, and aCI cohorts (n = 285, 92, and 529). The plasma antibody levels in the Japan Public Health Center-based Prospective Cohort Study (1991-1993) were also examined.
RESULTS
RESULTS
The candidate antigens were aldolase A (ALDOA) and fumarate hydratase (FH). In AlphaLISA, patients with TIA or aCI had higher anti-ALDOA antibody (ALDOA-Ab) and anti-FH antibody (FH-Ab) levels than the HDs (P < 0.05). In a multivariate logistic regression analysis, the ALDOA-Ab (odds ratio [OR]: 2.46, P = 0.0050) and FH-Ab (OR: 2.49, P = 0.0037) levels were independent predictors of TIA. According to the case-control study, the ALDOA-Ab (OR: 2.50, P < 0.01) and FH-Ab (OR: 2.60, P < 0.01) levels were associated with aCI risk. In a correlation analysis, both ALDOA-Abs and FH-Abs were well associated with hypertension, coronary heart disease, and habitual smoking. These antibody levels also correlated well with maximum intima-media thickness, which reflects atherosclerotic stenosis.
CONCLUSIONS
CONCLUSIONS
ALDOA-Abs and FH-Abs can be novel potential biomarkers for predicting atherosclerotic TIA and aCI.
Identifiants
pubmed: 34243715
doi: 10.1186/s12883-021-02301-w
pii: 10.1186/s12883-021-02301-w
pmc: PMC8268454
doi:
Substances chimiques
Autoantibodies
0
Biomarkers
0
ALDOA protein, human
EC 4.1.2.13
Fructose-Bisphosphate Aldolase
EC 4.1.2.13
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
274Subventions
Organisme : Natural Science Foundation of Guangdong Province
ID : 2018A0303131003
Organisme : Science and Technology Program of Guangzhou
ID : 201707010449
Organisme : Ministry of Health, Labour and Welfare and Ministry of Education, Culture, Sports, Science and Technology (MEXT)
ID : 20K17953
Organisme : Ministry of Health, Labour and Welfare and Ministry of Education, Culture, Sports, Science and Technology (MEXT)
ID : 17K16626
Organisme : Ministry of Health, Labour and Welfare of Japan
ID : Grant-in-Aid for Cancer Research
Organisme : Ministry of Health, Labour and Welfare of Japan
ID : 17K19810
Organisme : Ministry of Health, Labour and Welfare of Japan
ID : 19K09451
Informations de copyright
© 2021. The Author(s).
Références
Oncotarget. 2017 Dec 31;9(5):5600-5613
pubmed: 29464021
Microbiol Immunol. 2004;48(9):703-11
pubmed: 15383707
JAMA. 2002 Oct 23-30;288(16):2015-22
pubmed: 12387654
Int J Cancer. 2004 Dec 20;112(6):1029-35
pubmed: 15386348
Cell. 2012 Aug 17;150(4):685-96
pubmed: 22901803
Lancet. 2010 Jul 10;376(9735):112-23
pubmed: 20561675
Oncotarget. 2016 Oct 26;7(46):74526-74536
pubmed: 27793029
Metabolism. 2021 Mar;116:154461
pubmed: 33290761
Cancer Res. 2016 Jul 15;76(14):4259-4269
pubmed: 27261507
BMC Cancer. 2014 Jun 18;14:452
pubmed: 24946857
Methods Mol Med. 2005;109:137-54
pubmed: 15585919
Stroke. 2012 Apr;43(4):1013-7
pubmed: 22302109
Proc Natl Acad Sci U S A. 1984 May;81(9):2738-42
pubmed: 6585824
Jpn J Clin Oncol. 2014 Sep;44(9):777-82
pubmed: 25104790
Heliyon. 2020 Aug 19;6(8):e04661
pubmed: 32904265
Cell Mol Life Sci. 2018 Nov;75(22):4079-4091
pubmed: 29946805
Stroke. 2009 Jun;40(6):2276-93
pubmed: 19423857
Arch Intern Med. 2007 Dec 10;167(22):2417-22
pubmed: 18071162
BMC Neurol. 2015 Jul 28;15:119
pubmed: 26215720
Arthritis Res Ther. 2005;7(5):R1133-9
pubmed: 16207330
Circulation. 2003 Oct 7;108(14):1664-72
pubmed: 14530185
Curr Rheumatol Rep. 2009 Feb;11(1):61-9
pubmed: 19171113
J Neuroimmunol. 2015 Jul 15;284:30-6
pubmed: 26025055
BMC Med. 2014 Mar 18;12:47
pubmed: 24642015
Stroke. 2014 Jul;45(7):2160-236
pubmed: 24788967
Stroke. 2009 Feb;40(2):376-81
pubmed: 19095974
Nat Cell Biol. 2017 Jul;19(7):833-843
pubmed: 28628081
Cancer Lett. 2017 Sep 10;403:28-36
pubmed: 28610954
Asia Pac J Clin Nutr. 2008;17(1):8-16
pubmed: 18364320
J Transl Med. 2015 Feb 22;13:71
pubmed: 25890248
Stroke. 2000 Nov;31(11):2648-52
pubmed: 11062289
Genes Dev. 2012 Jun 15;26(12):1326-38
pubmed: 22677546
PLoS Biol. 2010 Mar 09;8(3):e1000328
pubmed: 20231875
Am J Physiol Heart Circ Physiol. 2012 Jul 15;303(2):H189-96
pubmed: 22661506
Biochem Biophys Res Commun. 2002 Jul 5;295(1):119-24
pubmed: 12083777
Int J Oncol. 2017 Feb;50(2):525-534
pubmed: 28000858
N Engl J Med. 1994 Dec 1;331(22):1474-9
pubmed: 7969297
Stroke. 2004 Aug;35(8):1842-6
pubmed: 15192239
J Circ Biomark. 2016 Apr 7;5:8
pubmed: 28936256
Stroke. 2013 Jul;44(7):2064-89
pubmed: 23652265
AJR Am J Roentgenol. 1992 Jul;159(1):191-7
pubmed: 1609697
Stroke. 2005 Apr;36(4):720-3
pubmed: 15731465
Stroke. 1993 Jan;24(1):35-41
pubmed: 7678184
Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11810-3
pubmed: 8524854
Front Oncol. 2012 Jul 31;2:85
pubmed: 22866264
Curr Protoc Immunol. 2005 Mar;Chapter 20:Unit 20.7
pubmed: 18432945
J Biol Chem. 1994 Sep 23;269(38):23757-63
pubmed: 8089148
Proc Natl Acad Sci U S A. 1995 Apr 25;92(9):3893-7
pubmed: 7732003
Eur Heart J. 2013 Apr;34(16):1225-32
pubmed: 23404536
Crit Care Med. 2017 Oct;45(10):e1011-e1017
pubmed: 28658027