Monocyte chemoattractant protein 1 gene regulatory region polymorphism and serum levels of monocyte chemoattractant protein 1 in Japanese patients with Kawasaki disease

Jibiki, Toshiaki; Terai, Masaru; Shima, Masayuki; Ogawa, Atsushi; Hamada, Hiromichi; Kanazawa, Masato; Yamamoto, Shozo; Oana, Shinji; Kohno, Yoichi

doi:10.1002/1529-0131(200109)44:9<2211::aid-art375>3.0.co;2-a

Cited by 72 publications

(36 citation statements)

References 8 publications

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“…11 Similarly, the MCP-1Ϫ2518A/G polymorphism influences the expression of the MCP-1 gene. 10,25 Also the Ϫ11715A/6A polymorphism of the MMP-3 gene promoter regulates transcription and protein levels in an allele-specific manner. 26 However, the 469 E/K polymorphism of the ICAM-1 gene results in a change in the amino acid sequence of the Ig-like domain 5, which is crucial for the interactions between ICAM-1 and LFA-1 and for the adhesion of B-cells.…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory Genetic Profiles in Subjects With History of Ischemic Stroke

Flex

Gaetani

Papaleo

et al. 2004

Stroke

148

100

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Background and Purpose-Proinflammatory genetic profiles, resulting from the combination of single nucleotide polymorphisms in genes encoding inflammatory molecules, may contribute to the development and progression of cardiovascular diseases. We evaluated the association between history of ischemic stroke and genetic profiles determined by the synergistic effects of polymorphisms in genes encoding prototypical inflammatory proteins. Methods-The study included 237 individuals with history of ischemic stroke and 223 age-matched and gender-matched controls. The polymorphisms of the C-reactive protein (CRP), interleukin-6 (IL-6), macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin (E-sel), and matrix metalloproteinase-3 (MMP-3) genes were studied. Results-IL-6 GG, IL-6 GC, MCP-1 GG, ICAM-1 EE, E-sel AA, and MMP-3 5A5A genotypes were significantly and independently associated with stroke history. The odds of stroke increased with the number of high-risk genotypes: carrying 1 proinflammatory gene variant conferred a risk of 3.3 (1.6 to 6.9), whereas individuals concomitantly carrying 2 and 3 proinflammatory gene variants had adjusted odds ratios of 21.0 (7.6 to 57.5) and 50.3 (10.2 to 248.1), respectively. Conclusions-Proinflammatory genetic profiles are significantly more common in subjects with stroke history. Synergistic effects between proinflammatory genotypes might be potential markers for cerebrovascular diseases.

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Section: Discussionmentioning

confidence: 99%

Proinflammatory Genetic Profiles in Subjects With History of Ischemic Stroke

Flex

Gaetani

Papaleo

et al. 2004

Stroke

148

100

View full text Add to dashboard Cite

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“…The effect of functional MCP-1 polymorphisms has been described in autoimmune and inflammatory disorders (20,21) and has been shown to predict the survival of renal transplants (22). The role of MCP-1 polymorphisms in SLE has been studied by other investigators, but has led to differing conclusions.…”

Section: Discussionmentioning

confidence: 99%

Strong association of a functional polymorphism in the monocyte chemoattractant protein 1 promoter gene with lupus nephritis

Tucci¹,

Barnes²,

Sobel³

et al. 2004

Arthritis & Rheumatism

121

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Objective. Lupus nephritis (LN) is a major contributor to morbidity and mortality in patients with systemic lupus erythematosus (SLE). There is evidence that polymorphisms in the genes of inflammatory mediators may predispose to the development of LN in patients with SLE. In this study, we examined the role of a functional monocyte chemoattractant protein 1 (MCP-1) polymorphism in SLE and LN.Methods. DNA and paired urine and serum samples were obtained from 134 SLE patients (>4 American College of Rheumatology criteria for SLE; 49 with and 85 without LN) and 118 controls. MCP-1 genomic variants were detected by polymerase chain reaction followed by restriction enzyme-fragment analysis. Urinary and serum MCP-1 levels and MCP-1 production by peripheral blood macrophages were measured by enzyme-linked immunosorbent assay.Results. The A/A genotype was more common in controls than in SLE patients (P ‫؍‬ 0.0002), whereas both the A/G (P ‫؍‬ 0.009) and G/G (P ‫؍‬ 0.0212) genotypes were more frequent in SLE patients. The A/A genotype was observed in only 23% of the patients with LN compared with 58% of those without LN (P < 0.0001). MCP-1 production by peripheral blood mononuclear cells from patients with the A/G and G/G phenotypes was markedly higher than the production by cells from patients with the A/A genotype. Urinary levels of MCP-1 were significantly higher in patients with LN.Conclusion. These results suggest that an A/G or G/G genotype may predispose to the development of SLE and further indicate that SLE patients with these genotypes may be at higher risk of developing LN. Moreover, measurement of urinary levels of MCP-1 may be a useful tool for the detection and management of LN.

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“…30 Although several other groups have studied other combinations of HLA subtypes, no consistent association has been detected so far. Considering that no significant linkage was detected near the 6p region in our genome-wide linkage analysis, 31 34 and MCP-1 35 ), hematopoietins (interleukin-4 (IL-4) [36][37][38] and IL-6 39 ), IL-1 family (IL-1b, 37 IL-18, 40 and IL-1Ra 37 ), IL-10 family (IL-10 41 ), platelet-derived growth factor family (vascular endothelial growth factor (VEGF) [42][43][44][45] and VEGFR2 42 ), and tumor necrosis factor (TNF) family (TNF-a, 46-50 lipoteichoic acid, 47 and CD40L 51,52 ). Other candidates include plasma proteins (C-reactive protein [53][54][55] and MBL2 53,55,56 ), matrix metalloproteinase (MMP) and their inhibitors (MMP2, 58 MMP3, 57,58 MMP-9, 58 MMP-12, 58 MMP-13, 58 and tissue inhibitors of metalloproteinase-2 59 ), enzymes related to atherosclerosis (methylenetetrahydrofolate reductase (MTHFR), 60 endothelial nitric oxide synthase, 61 and inducible nitric oxide synthase 61 ), components of the renin-angiotensin system (angiotensin-converting enzyme [62][63][64][65] and AGTR1 64 ), and an unclassified group (CD14, 66 FCGR2A, 67,68 SLC11A1, 69 PLA2G7, 70 UGT1A1, 71 MICA, 72 and HMOX1 71 ).…”

Section: Candidate Gene Approachmentioning

confidence: 90%

Susceptibility genes for Kawasaki disease: toward implementation of personalized medicine

Hata

Onouchi

2009

J Hum Genet

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Kawasaki disease (KD) is an acute systemic vasculitis syndrome, which primarily affects in children under the age of 5 years. In 20-25% of cases, if untreated, coronary artery lesions develop, making KD the leading cause of acquired heart disease in children in both Japan and the United States. Since 1970, 19 nationwide surveys of KD in Japan have been conducted every 2 years and the data are stored in a database. Even though the etiology of KD remains unknown, despite enthusiastic research spanning more than 40 years, we have learnt a great deal about KD from this enormous database. These 19 epidemiologic studies indicate a strong genetic influence on the disease susceptibility, prompting us and other researchers to identify the responsible genes for KD by applying either the candidate gene approach or the genome-wide approach. We have employed a genome-wide linkage study using affected sibling pair data of KD in Japan and have identified several susceptibility loci. Further analysis focusing on a region of chromosome 19, where one of the linked loci was detected, identified a predisposing gene, which codes inositol 1,4,5-trisphosphate 3-kinase C (ITPKC). In this review, we summarize the cumulative knowledge regarding KD, and then outline our hypothesis of the role ITPKC plays in KD susceptibility and our trial that aims toward the implementation of personalized medicine for KD.

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Monocyte chemoattractant protein 1 gene regulatory region polymorphism and serum levels of monocyte chemoattractant protein 1 in Japanese patients with Kawasaki disease

Cited by 72 publications

References 8 publications

Proinflammatory Genetic Profiles in Subjects With History of Ischemic Stroke

Proinflammatory Genetic Profiles in Subjects With History of Ischemic Stroke

Strong association of a functional polymorphism in the monocyte chemoattractant protein 1 promoter gene with lupus nephritis

Susceptibility genes for Kawasaki disease: toward implementation of personalized medicine

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