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

Zoltan Szolnoki, Anita Maasz, Lili Magyari, Katalin Horvatovich, Bernadett Farago, Andras Kondacs, Anita Bodor, Ferenc Hadarits, Peter Orosz, Alexandru Ille, Bela Melegh

Research output: Contribution to journalArticle

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 - Apr 2009

Keywords

  • Galectin-2
  • Genetic interaction
  • LGALS2 3279TT variant
  • LTA 252GG
  • Lymphotoxin-alpha
  • Stroke

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology

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