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A Novel Association of the Suppressor of Cytokine Signaling 1 (SOCS1) Gene Polymorphisms in Ischemic Stroke Patients

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Abstract

Ischemic stroke is a common neurological disease and a leading cause of permanent disability in many countries. Recent studies provide evidence on the role of the suppressor of the cytokine signaling 1 (SOCS1) gene in the development and progression of atherosclerotic lesions. However, few studies have assessed the association between single nucleotide polymorphisms (SNPs) on SOCS1 gene and ischemic stroke. Therefore, the present study aimed to investigate the role of SOCS1 polymorphism in ischemic stroke risk in a northern Chinese Han population. We examined 475 patients with ischemic stroke and 486 normal controls. Three SNPs (rs243327, rs243330, and rs33932899) of SOCS1 gene were determined for TaqMan genotyping assays. We also classified these case samples in depth by complications with hypertension or diabetes and by ischemic stroke subtypes. When adjusting models by multiple factor analysis by logistic regression, then calculated 10,000 permutations were performed for each model to correct the multiple test. Under additive model, the rs243327 was associated with ischemic stroke with hypertension (p = 0.047). Under heterozygous model, the rs33932899 and rs243330 were significantly associated with ischemic stroke subtypes by atherosclerosis (p = 0.038, p = 0.048, respectively). In summary, our data demonstrated for the first time that the polymorphisms of the SOCS1 gene are associated with the risk of ischemic stroke in a northern Chinese Han population, suggesting that SOCS1 gene polymorphisms may play an important role in the pathogenesis of ischemic stroke.

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Acknowledgments

This work was supported by the Natural Science Foundation of Heilongjiang province (No. H201331).

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Correspondence to Litao Sun.

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Qi Ma and Nana Liu: Co first authors.

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Ma, Q., Liu, N., Zhang, R. et al. A Novel Association of the Suppressor of Cytokine Signaling 1 (SOCS1) Gene Polymorphisms in Ischemic Stroke Patients. Neuromol Med 18, 573–580 (2016). https://doi.org/10.1007/s12017-016-8406-x

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  • DOI: https://doi.org/10.1007/s12017-016-8406-x

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