Evidence map›Paper›PMID 23242661›Full record

ArticleMolecular biology reports2013

ICAM1 K469E and E-selectin S128R polymorphisms could predispose to increased autoantibody production and TSH suppression in Graves' disease.

Müge Kanmaz-Özer, Semra Doğru-Abbasoğlu, Pervin Vural, Ayşenur Özderya, Berrin Karadağ, Müjdat Uysal

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Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
0.5field-weighted citation impact, top 39% of its field
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3 · Its place in the literature

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1 citing paper in PubMed, 5 citations in OpenAlex.

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5 · Who and what money

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6 authors at 1 institution in 1 country.

Müge Kanmaz-ÖzerDepartment of Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Çapa, 34093, Istanbul, Turkey.
Semra Doğru-Abbasoğlu
Pervin Vural
Ayşenur Özderya
Berrin Karadağ
Müjdat Uysal
Istanbul University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiopathogenesis of Graves' disease (GD) has not been clearly elucidated although the role of chronical inflammation and endothelial dysfunction has been established. Adhesion molecules such as intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), and E-selectin are secreted from vascular endothelium and promote accumulation of leukocytes in damaged endothelial areas. This study examined the possible association of ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) single nucleotide polymorphisms (SNPs) with the occurrence of GD. ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs in DNA from peripheral blood leukocytes of 171 patients with GD and 259 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. We did not find significant differences in the distributions of studied polymorphisms, nor in the haplotype frequencies between patients with GD and healthy control. However, the anti-TPO levels in E-selectin 128R allele carrying subjects (SR + RR) were higher than S128S genotype (p < 0.05). In addition, the decline of TSH levels was more prominent in ICAM1 469 E carrying subjects (KE + EE) in comparison with wild homozygotes (p < 0.05). Although there is not association between ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs and susceptibility to GD, higher anti-TPO in E-selectin 128 SR + RR, and lower TSH in ICAM1 469 KE + EE subjects suspect that these genotypes are prone to increased antithyroid autoantibody production with more accentuated TSH suppression in GD. Further studies with a larger cohort, analyzing other polymorphisms in ICAM, VCAM1 and E-selectin genes are necessary to support our observations.

Indexed as

Polymorphism, GeneticAdolescentAdultAgedAllelesAutoantibodiesCase-Control StudiesE-SelectinFemaleGene FrequencyGenotypeGraves DiseaseHaplotypesHumansIntercellular Adhesion Molecule-1MaleAutoantibodiesE-SelectinIntercellular Adhesion Molecule-1Thyrotropin

Identifiers

PMID23242661
OpenAlexW1965065196

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.