Susceptibility for ischemic stroke in Korean population is associated with polymorphisms of the interleukin-1 receptor antagonist and tumor necrosis factor-α genes, but not the interleukin-1β gene

Lee, Byung-Cheol; Ahn, Sung-Ho; Doo, Ho-Kyung; Yim, Sung-Vin; Lee, Hee-Jae; Jin, Sheng‐Yu; Hong, Seung‐Jae; Lee, Sang-Ho; Kim, Sung-Do; Jung-Chul, Seo; Leem, Kang‐Hyun; Chung, Joo‐Ho

doi:10.1016/j.neulet.2003.12.041

Cited by 58 publications

(35 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In vitro studies have shown that the TNF- α– 308A variant in the promoter region plays a functional role in increasing the transcriptional activity and elevated plasma TNF-α levels [12,13]. Our results suggest a difference based on gender, which is in agreement with the report by Lee et al [24], showing that the TNF- α–308GG genotype is significantly higher in male ischemic stroke patients. Experimental stroke studies in animals have also shown that there are gender differences in the outcome of cerebral ischemia [29,30].…”

Section: Discussionsupporting

confidence: 92%

See 1 more Smart Citation

Association between Tumor Necrosis Factor-Alpha (–308G→A and –238G→A) Polymorphisms and Homocysteine Levels in Patients with Ischemic Strokes and Silent Brain Infarctions

et al. 2010

View full text Add to dashboard Cite

Background and Purpose: The aims of this study were to evaluate the role of tumor necrosis factor-α (TNF-α) polymorphisms in patients susceptible to ischemic stroke and silent brain infarction (SBI), and to determine the relationship between TNF-α polymorphisms and plasma total homocysteine (tHcy) levels. Methods: We studied 237 patients with ischemic stroke, 257 patients with SBIs, and 216 control subjects. For control subjects, we selected healthy individuals matched for gender and age from those individuals who came to our hospital for health examinations. The TNF-α–308G→A and –238G→A genotypes were determined by the polymerase chain reaction-restriction fragment length polymorphism method. Results: The frequency of the TNF-α–308G→A polymorphism was significantly different between the patients with ischemic stroke and the control group (GG vs. GA+AA; adjusted odds ratio, AOR, 0.50; 95% CI 0.255–0.989). By subgroup analysis, when tHcy levels were stratified into high (>10.80 µmol/l), moderate (8.21–10.80 µmol/l), and low levels (<8.21 µmol/l), the frequency of the TNF-α–308GA+AA genotype in the highest tertile group was higher than in the lowest tertile group (AOR 2.46; 95% CI 1.063–5.699). However, the relationship between SBI susceptibility and polymorphisms of TNF-αwas not established. The tHcy levels were significantly and inversely correlated with folate levels in the TNF-α–308GG and TNF-α–238GG genotypes in the ischemic stroke, SBI, and control groups (p< 0.05). Conclusions: Our results suggest that the TNF-α–308G→A polymorphism is responsible for susceptibility to ischemic stroke and is associated with high tHcy levels in Koreans.

show abstract

Section: Discussionsupporting

confidence: 92%

“…This result is supported by reports by other investigators [23,24,25,26,27]. Um and Kim [23] reported that the TNF- α –308A allele of the promoter polymorphism was significantly decreased in patients with cerebral infarction compared to the controls among the Korean population.…”

Section: Discussionsupporting

confidence: 86%

Association between Tumor Necrosis Factor-Alpha (–308G→A and –238G→A) Polymorphisms and Homocysteine Levels in Patients with Ischemic Strokes and Silent Brain Infarctions

et al. 2010

View full text Add to dashboard Cite

show abstract

“…29 Furthermore, studies of the IL-1 and IL-1RA genes suggest that polymorphisms in both IL-1a and IL-1RA genes may be associated with increased risk of stroke. [30][31][32] Similarly, TNF-a has been hypothesized to play an important role in neurodegeneration. 33 TNF-a release from blood cells and serum levels of TNF-a were found to be elevated during the acute phase following stroke compared with healthy controls.…”

Section: Resultsmentioning

confidence: 99%

“…[34][35][36] Furthermore, increased levels of TNF-a in the cerebral spinal fluid and serum of acute stroke patients has been associated with increased severity of postischemic neuropathology 37 and polymorphism of the TNF gene have been associated with susceptibility to ischemic stroke. 32 IL-6 is a pleiotropic cytokine involved in inflammatory processes and like IL-1 is able to induce acute inflammatory responses such as fibrinogen and C-reactive protein production. The C-reactive protein, an important peripheral inflammatory marker, is strongly associated with risk for stroke.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2006

View full text Add to dashboard Cite

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.

show abstract

“…Unlike Dutch [42] and Finnish subjects [43], in a population of Korean origin, few cases bore the IL-1a-889 A2/A2 genotype (0.8% instead of 10.0 and 8% found in Dutch and Finnish subject respectively) [44]. In case of ischemic stroke patients, several groups have reported that no significant association was seen for the IL-1b (-511) polymorphism [45][46][47]. Zee et al [48] reported that the IL-1a (-889) was not associated with the susceptibility to ischemic stroke.…”

Section: Polymorphisms Of the Il-1 Clustermentioning

confidence: 97%

Aspects of gene polymorphisms in cerebral infarction: inflammatory cytokines

Jeong

Park

et al. 2005

CMLS, Cell. Mol. Life Sci.

View full text Add to dashboard Cite

During the last decade, a growing corpus of evidence has indicated an important role of inflammatory cytokines in the pathogenesis of cerebral lesion following stroke. Recent data suggest that genetics may in turn contribute to modulating the effects of inflammatory cytokines on cerebral infarction (CI). This paper reviews the physiologic characteristics of major inflammatory cytokines and recent research developments related to cell biology and pathobiology in CI. In particular, this review focuses on the genetic aspects of inflammatory cytokines and their implications in CI.

show abstract

Susceptibility for ischemic stroke in Korean population is associated with polymorphisms of the interleukin-1 receptor antagonist and tumor necrosis factor-α genes, but not the interleukin-1β gene

Cited by 58 publications

References 18 publications

Association between Tumor Necrosis Factor-Alpha (–308G→A and –238G→A) Polymorphisms and Homocysteine Levels in Patients with Ischemic Strokes and Silent Brain Infarctions

Association between Tumor Necrosis Factor-Alpha (–308G→A and –238G→A) Polymorphisms and Homocysteine Levels in Patients with Ischemic Strokes and Silent Brain Infarctions

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

Aspects of gene polymorphisms in cerebral infarction: inflammatory cytokines

Contact Info

Product

Resources

About