Galectin-2 3279TT variant protects against the lymphotoxin-α 252GG genotype associated ischaemic stroke

Z. Szolnoki, A. Maász, L. Magyari, Katalin Horvatovich, Bernadett Farago, A. Kondacs, Anita Bodor, Ferenc Hadarits, Peter Orosz, Alexandru Ille, B. Melegh

Research output: Article

8 Citations (Scopus)

Abstract

Objective: The galectin-2 protein is presumed to play a regulatory role in the intracellular trafficking of the lymphotoxin-α (LTA) cytokine. LTA is a pro-inflammatory factor, its 252GG homozygote variant is considered as a susceptibility factor for arteriosclerosis and cardiovascular diseases. By contrast, the galectin-2-encoding gene LGALS2 3279TT homozygote variant has been demonstrated to exert protection against myocardial infarction by reducing the transcriptional level of galectin-2, thereby leading to a reduced extracellular secretion of LTA. Methods: In the present study, we examined whether the LGALS2 3279TT homozygote variant alone can influence the prevalence of ischaemic stroke, and whether it can interact somehow with the disadvantageous LTA 252GG homozygote variant. Genetic and clinical data of 385 ischemic stroke patients and 303 stroke and neuroimaging alteration-free controls were analysed. Results: The combination of the LGALS2 3279TT and LTA 252GG homozygote was significantly less frequent in the ischemic stroke group (1.56%) than in the controls (5.94%, p <0.00187; overall stroke group: crude OR: 0.25, 95% CI: 0.1-0.64; adjusted OR: 0.03, 95% CI: 0.025-0.71). Conclusions: This finding suggests a gene-gene interaction.

Original languageEnglish
Pages (from-to)227-230
Number of pages4
JournalClinical Neurology and Neurosurgery
Volume111
Issue number3
DOIs
Publication statusPublished - ápr. 2009

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Galectin 2
Lymphotoxin-alpha
Homozygote
Stroke
Genotype
Genes
Arteriosclerosis
Neuroimaging
Cardiovascular Diseases
Myocardial Infarction
Cytokines

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Galectin-2 3279TT variant protects against the lymphotoxin-α 252GG genotype associated ischaemic stroke. / Szolnoki, Z.; Maász, A.; Magyari, L.; Horvatovich, Katalin; Farago, Bernadett; Kondacs, A.; Bodor, Anita; Hadarits, Ferenc; Orosz, Peter; Ille, Alexandru; Melegh, B.

In: Clinical Neurology and Neurosurgery, Vol. 111, No. 3, 04.2009, p. 227-230.

Research output: Article

Szolnoki, Z. ; Maász, A. ; Magyari, L. ; Horvatovich, Katalin ; Farago, Bernadett ; Kondacs, A. ; Bodor, Anita ; Hadarits, Ferenc ; Orosz, Peter ; Ille, Alexandru ; Melegh, B. / Galectin-2 3279TT variant protects against the lymphotoxin-α 252GG genotype associated ischaemic stroke. In: Clinical Neurology and Neurosurgery. 2009 ; Vol. 111, No. 3. pp. 227-230.
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abstract = "Objective: The galectin-2 protein is presumed to play a regulatory role in the intracellular trafficking of the lymphotoxin-α (LTA) cytokine. LTA is a pro-inflammatory factor, its 252GG homozygote variant is considered as a susceptibility factor for arteriosclerosis and cardiovascular diseases. By contrast, the galectin-2-encoding gene LGALS2 3279TT homozygote variant has been demonstrated to exert protection against myocardial infarction by reducing the transcriptional level of galectin-2, thereby leading to a reduced extracellular secretion of LTA. Methods: In the present study, we examined whether the LGALS2 3279TT homozygote variant alone can influence the prevalence of ischaemic stroke, and whether it can interact somehow with the disadvantageous LTA 252GG homozygote variant. Genetic and clinical data of 385 ischemic stroke patients and 303 stroke and neuroimaging alteration-free controls were analysed. Results: The combination of the LGALS2 3279TT and LTA 252GG homozygote was significantly less frequent in the ischemic stroke group (1.56{\%}) than in the controls (5.94{\%}, p <0.00187; overall stroke group: crude OR: 0.25, 95{\%} CI: 0.1-0.64; adjusted OR: 0.03, 95{\%} CI: 0.025-0.71). Conclusions: This finding suggests a gene-gene interaction.",
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AU - Szolnoki, Z.

AU - Maász, A.

AU - Magyari, L.

AU - Horvatovich, Katalin

AU - Farago, Bernadett

AU - Kondacs, A.

AU - Bodor, Anita

AU - Hadarits, Ferenc

AU - Orosz, Peter

AU - Ille, Alexandru

AU - Melegh, B.

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N2 - Objective: The galectin-2 protein is presumed to play a regulatory role in the intracellular trafficking of the lymphotoxin-α (LTA) cytokine. LTA is a pro-inflammatory factor, its 252GG homozygote variant is considered as a susceptibility factor for arteriosclerosis and cardiovascular diseases. By contrast, the galectin-2-encoding gene LGALS2 3279TT homozygote variant has been demonstrated to exert protection against myocardial infarction by reducing the transcriptional level of galectin-2, thereby leading to a reduced extracellular secretion of LTA. Methods: In the present study, we examined whether the LGALS2 3279TT homozygote variant alone can influence the prevalence of ischaemic stroke, and whether it can interact somehow with the disadvantageous LTA 252GG homozygote variant. Genetic and clinical data of 385 ischemic stroke patients and 303 stroke and neuroimaging alteration-free controls were analysed. Results: The combination of the LGALS2 3279TT and LTA 252GG homozygote was significantly less frequent in the ischemic stroke group (1.56%) than in the controls (5.94%, p <0.00187; overall stroke group: crude OR: 0.25, 95% CI: 0.1-0.64; adjusted OR: 0.03, 95% CI: 0.025-0.71). Conclusions: This finding suggests a gene-gene interaction.

AB - Objective: The galectin-2 protein is presumed to play a regulatory role in the intracellular trafficking of the lymphotoxin-α (LTA) cytokine. LTA is a pro-inflammatory factor, its 252GG homozygote variant is considered as a susceptibility factor for arteriosclerosis and cardiovascular diseases. By contrast, the galectin-2-encoding gene LGALS2 3279TT homozygote variant has been demonstrated to exert protection against myocardial infarction by reducing the transcriptional level of galectin-2, thereby leading to a reduced extracellular secretion of LTA. Methods: In the present study, we examined whether the LGALS2 3279TT homozygote variant alone can influence the prevalence of ischaemic stroke, and whether it can interact somehow with the disadvantageous LTA 252GG homozygote variant. Genetic and clinical data of 385 ischemic stroke patients and 303 stroke and neuroimaging alteration-free controls were analysed. Results: The combination of the LGALS2 3279TT and LTA 252GG homozygote was significantly less frequent in the ischemic stroke group (1.56%) than in the controls (5.94%, p <0.00187; overall stroke group: crude OR: 0.25, 95% CI: 0.1-0.64; adjusted OR: 0.03, 95% CI: 0.025-0.71). Conclusions: This finding suggests a gene-gene interaction.

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