Synergistic Effect of −174 G/C Polymorphism of the Interleukin-6 Gene Promoter and 469 E/K Polymorphism of the Intercellular Adhesion Molecule-1 Gene in Italian Patients With History of Ischemic Stroke

Pola, Roberto; Flex, Andrea; Gaetani, Eleonora; Flore, Roberto; Serricchio, Michele; Pola, Paolo

doi:10.1161/01.str.0000062346.70983.df

Cited by 100 publications

(79 citation statements)

References 31 publications

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“…However, epidemiological data on the association of the IL-6 gene polymorphism with ischemic stroke, subtypes and intermediate phenotypes are conflicting. Pola et al [33] observed an increased risk of ischemic stroke in carriers of the IL-6 GG genotype (OR=8.6), which is in agreement with the results of Stefan Greisenegger [34] . Rundek et al also revealed that the G allele confers an increased risk of IMT [35] .…”

Section: Ischemic Strokesupporting

confidence: 80%

Genetics of stroke

Guo

Liu

2010

Acta Pharmacol Sin

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Stroke is the second most common cause of death and the most common cause of disability in developed countries. Stroke is a multifactorial disease caused by a combination of environmental and genetic factors. Numerous epidemiologic studies have documented a significant genetic component in the occurrence of strokes. Genes encoding products involved in lipid metabolism, thrombosis, and inflammation are believed to be potential genetic factors for stroke. Although a large group of candidate genes have been studied, most of the epidemiological results are conflicting. Studies of stroke as a monogenic disease have made huge progress, and animal models serve as an indispensable tool to dissect the complex genetics of stroke. In the present review, we provide insight into the role of in vivo stroke models for the study of stroke genetics.

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Section: Ischemic Strokesupporting

confidence: 80%

Genetics of stroke

Guo

Liu

2010

Acta Pharmacol Sin

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“…21,38 -49 We excluded 1 article published in Chinese; this casecontrol study found the GG genotype to be significantly more frequent in transient ischemic attack patients and to be predictive of subsequent ischemic stroke within 3 months. 49 Three of the remaining 12 articles reported on a subset of patients from a later publication (confirmed by the listed corresponding authors), 41,46,47 leaving 9 unique patient populations (Table). No additional references were found from the bibliographies of the selected articles.…”

Section: Resultsmentioning

confidence: 97%

Interleukin-6 −174G/C Polymorphism and Ischemic Stroke

Tso

Merino

Warach

2007

Stroke

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Background and Purpose-Interleukin-6 (IL-6) is associated with atherosclerotic disease and is also a key mediator in the inflammatory response to cerebral ischemia. Although the IL-6 Ϫ174G/C promoter polymorphism has been associated with carotid artery atherosclerosis and coronary heart disease, its relation to ischemic stroke is unclear. This review summarizes the current literature and discusses methodological considerations for future studies. Methods-Electronic searches were conducted in the PubMed MEDLINE, Scopus, and ISI Web of Science databases. Two investigators independently reviewed all abstracts to identify studies examining the association between the IL-6 Ϫ174G/C polymorphism and ischemic cerebrovascular events. Results-Twelve relevant publications were identified. Three reported on a subset of patients from a later publication, leaving 9 independent studies. Two studies found an association between ischemic stroke and the G allele or GG genotype, whereas 4 found an association with the C allele or CC genotype. One study found the CC genotype to be significantly less frequent in retinal artery occlusion patients. Two studies found no association between the Ϫ174G/C polymorphism and stroke. Conclusions-Studies investigating stroke and the Ϫ174G/C polymorphism report conflicting results, which may reflect the complex physiology of IL-6 and true differences between stroke subtypes and populations. However, interpretation of published results is hindered by methodological limitations, and greater rigor and consistency in future studies will help unravel the relationship between the Ϫ174G/C polymorphism and stroke. (Stroke.

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“…[38][39][40] Although a clear picture of the role of IL-6 in stroke has not yet been elucidated, an increase in IL-6 production following cerebral ischemia has been described in several clinical studies 21,34,41,42 and elevated levels of the IL-6 cytokine have been correlated with severity and clinical outcome of stroke. 28,43,44 Furthermore, polymorphisms of the promoter IL-6 gene have been associated with stroke 45,46 and the IL-6 system has been associated with acute inflammatory response after stroke. 47 In addition, the IL-8 chemokine has also been associated with the recruitment of inflammatory cells and is increased in stroke patients.…”

Section: Resultsmentioning

confidence: 99%

The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

et al. 2006

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Although poststroke depression is unlikely to represent a single disorder and numerous etiologies for different kinds of poststroke depression will likely emerge as the result of future research, we believe that a number of poststroke depressive disorders are likely to be the result of specific changes in brain pathology and neurophysiology. Nevertheless, there are relatively few hypotheses about the pathophysiology of poststroke depression. This paper, therefore, proposes a new hypothesis for poststroke depression involving increased production of proinflammatory cytokines resulting from brain ischemia in cerebral areas linked to the pathogenesis of mood disorders. This paper reviews the evidence supporting the hypothesis that proinflammatory cytokines are involved in the occurrence of stroke as well as mood disorders linked to the brain damage. The increased production of proinflammatory cytokines such as IL-1b, TNF-a or IL-18 resulting from stroke may lead to an amplification of the inflammatory process, particularly in limbic areas, and widespread activation of indoleamine 2,3-dioxygenase (IDO) and subsequently to depletion of serotonin in paralimbic regions such as the ventral lateral frontal cortex, polar temporal cortex and basal ganglia. The resultant physiological dysfunction may lead to poststroke depression. Future investigations may explore this hypothesis through more extensive studies on the role of proinflammatory cytokines, such as IL-1b, TNF-a or even IL-18, in patients with poststroke depression. Molecular Psychiatry (2006) 11, 984-991.

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Synergistic Effect of −174 G/C Polymorphism of the Interleukin-6 Gene Promoter and 469 E/K Polymorphism of the Intercellular Adhesion Molecule-1 Gene in Italian Patients With History of Ischemic Stroke

Cited by 100 publications

References 31 publications

Genetics of stroke

Genetics of stroke

Interleukin-6 −174G/C Polymorphism and Ischemic Stroke

The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

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