Genetic polymorphisms of RAGE and risk of ulcerative colitis in a Chinese population

Wang, Jiafeng; Zeng, Juncheng; Wang, Hao; Ye, Shicai; Bi, Ye; Zhou, Yunyun; Li, Keshen; Zhou, Yu

doi:10.1016/j.imlet.2015.09.003

Cited by 13 publications

(7 citation statements)

References 40 publications

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“…Thus, TLR4 KO mice are more susceptible to experimental colitis, and similar results have been obtained for a number of TLRs and related genes (Sánchez de Medina et al, ). In turn, RAGE has been linked to colitis or IBD, as well as colitis‐related cancer, and has been suggested to be involved in leukocyte transepithelial migration (Wang et al, ). However, RAGE KO mice show no change in sensitivity to DSS colitis (Däbritz et al, ).…”

Section: Discussionmentioning

confidence: 99%

Calprotectin protects against experimental colonic inflammation in mice

Aranda

Ocón

Arredondo-Amador

et al. 2018

British J Pharmacology

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Section: Discussionmentioning

confidence: 99%

Calprotectin protects against experimental colonic inflammation in mice

Aranda

Ocón

Arredondo-Amador

et al. 2018

British J Pharmacology

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“…One preliminary case-control study found a correlation between the G82S allele in RAGE and UC risk in a Chinese population. However, no correlation between polymorphisms in the RAGE promoter region and UC risk were observed [27] . In the present study, we investigated the RAGE promoter methylation status and found no significant correlation between promoter methylation and UC risk.…”

Section: Discussionmentioning

confidence: 99%

“…However, few studies have addressed the correlation between RAGE promoter methylation and UC risk. Previously, Wang (2016) found a significant correlation between RAGE single-nucleotide polymorphisms (G82S) and UC risk in a Chinese population [27] . However, no correlation was found between UC risk and two SNPs in the RAGE promoter region, which were expected to have an important effect on RAGE transcription in early stages of the disease.…”

Section: Introductionmentioning

confidence: 99%

Promoter methylation cooperates with SNPs to modulate RAGE transcription and alter UC risk

Wang

Yan

Zhou

et al. 2019

Biochemistry and Biophysics Reports

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Single-nucleotide polymorphisms (SNPs) located in the promoter region of the receptor for advanced glycation end products (RAGE) gene have been linked to the activity of RAGE. However, contrary to our expectation, we previously detected no correlation between SNPs within the RAGE promoter and ulcerative colitis (UC) risk in a case-control study. Here, we investigated the methylation of the RAGE promoter and analyzed the collective contribution of methylation and SNPs to UC risk. We found that RAGE promoter hypomethylation was more common in UC patients compared to controls (70% vs. 30%, respectively), as determined via bisulfite sequencing PCR (BSP) and methylation-specific PCR (MSP). Furthermore, we investigated the cooperativity of promoter methylation and SNPs and found that either of two SNPs (rs1800624 or rs1800625) and promoter methylation jointly contributed to UC risk (30 UC patients vs. 30 controls, P < 0.05). There was no correlation between UC risk and either methylation or SNPs when analyzed separately. This lack of correlation is likely due to promoter methylation repressing gene transcription, whereas SNPs in the RAGE promoter region activate RAGE transcription. We found that variant allele carriers with promoter hypomethylation were at an increased risk for UC (rs1800624, OR = 10, 95% CI: 1.641–60.21, P = 0.009; rs1800625, OR = 4.8, 95% CI: 1.074–21.447, P = 0.039). Furthermore, our data revealed that the RAGE mRNA levels in variant allele carriers with promoter hypomethylation were significantly higher compared to those with promoter hypermethylation (P < 0.05) as well as to those in wild-type allele individuals exhibiting promoter hypomethylation (P < 0.05). We therefore speculate that the methylation status and SNPs present in the RAGE promoter region alter RAGE transcription, thereby impacting UC risk. We also propose that the methylation status and RAGE promoter genotype could jointly serve as clinical biomarkers to assist in UC risk assessment.

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“…Increasing evidence indicated that RAGE is upregulated in sepsis , thus it is tempting to infer that the promoter polymorphisms of RAGE could alter transcription which leads to increased RAGE expression levels and different disease outcomes. In fact, several functional polymorphisms of RAGE have been reported to alter transcription in many diseases . Moreover, several studies reported that −374T>A and −429T>C polymorphisms exhibited higher RAGE expression levels and increased susceptibility to some diseases such as aspergillosis and diabetic retinopathy , while others suggested that the −374A and −429C alleles might lead to less RAGE expression and played a protective effect on many diseases .…”

Section: Discussionmentioning

confidence: 99%

The promoter polymorphisms of receptor for advanced glycation end products were associated with the susceptibility and progression of sepsis

Shao

et al. 2016

Clinical Genetics

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Receptor for advanced glycation end products (RAGE) is considered a major pattern recognition receptor, which plays an important role in the development of sepsis. Increasing evidence showed an association between RAGE polymorphisms and the susceptibility to several inflammatory-related diseases. However, little is known about the clinical relationship between RAGE polymorphisms and sepsis. In this study, we analyzed the association of sepsis with three functional RAGE gene polymorphisms (rs1800624, rs1800625 and rs2070600) in a Chinese Han population (372 sepsis cases and 400 healthy controls). Significant differences were observed in the rs1800624 and rs1800625 genotype/allele distributions between the sepsis and controls, but no significant difference was observed in the rs2070600 genotype/allele. Moreover, our results also revealed a significant difference in the genotype/allele frequencies of the rs1800624 and rs1800625 polymorphisms between the sepsis and severe sepsis subtypes, the rs1800624 TT or rs1800625 TT genotype carriers exhibited a significant increase in RAGE mRNA, sRAGE, TNF-α and IL-6 expression compared with the rs1800624 AT/AA or rs1800625 CT/CC carriers in sepsis patients. Overall, this study might provide valuable clinical evidence between the RAGE gene polymorphisms and the risk or the development of sepsis.

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Genetic polymorphisms of RAGE and risk of ulcerative colitis in a Chinese population

Cited by 13 publications

References 40 publications

Calprotectin protects against experimental colonic inflammation in mice

Calprotectin protects against experimental colonic inflammation in mice

Promoter methylation cooperates with SNPs to modulate RAGE transcription and alter UC risk

The promoter polymorphisms of receptor for advanced glycation end products were associated with the susceptibility and progression of sepsis

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