Novel single nucleotide polymorphism of the <i>VEGF</i> gene as a risk predictor for gastroduodenal ulcers

Kim, Yong Seok; Park, Sang Woon; Kim, Min Ho; Jang, Eun Jeong; Park, Ju Sang; Park, Sang Jong; Baik, Hyun Wook; Chung, Gregory K. W. K.; Hahm, Ki Baik

doi:10.1111/j.1440-1746.2008.05404.x

Cited by 10 publications

(8 citation statements)

References 49 publications

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“…It has been demonstrated that the C936T SNP in the 3'-UTR of the VeGF gene is associated with a reduced serum level of cytokine (69,70). More recently, a novel SNP in the VeGF promoter (-1780 T/C), which was found to significantly affect gene expression, has been described (67). The authors reported a strong relationship between this SNP and the occurrence of gastroduodenal ulcers.…”

Section: Tnf Gene Variantsmentioning

confidence: 81%

“…Moreover, they confirmed that the transfection of the HMeC-1 endothelial cell line with the -1780 T/C SNP-containing vector influenced the angiogenic activity of these cells in vitro. Indeed, cells transfected with this mutant vector displayed repressed promoter activity as compared to cells transfected with the wild-type vector, and subsequently displayed impaired angiogenic potential (67).…”

Section: Tnf Gene Variantsmentioning

confidence: 99%

“…Impaired angiogenesis resulting from genetically determined abnormalities in the VeGF expression level or cytokine structure itself has been observed in various pathologies (66). Therefore, the highly polymorphic VeGF gene has been the subject of numerous studies concerning the role of VeGF gene variants in diabetes complications, rheumatoid arthritis, renal allograft rejection, psoriasis, endometriosis, gastroduodenal ulcers and various cancers (67)(68)(69). Among various polymorphisms in the VeGF gene studied to date, two were found to be significantly associated with impaired expression of this cytokine, and thus could be considered potent risk factors of impaired chronic wound healing.…”

Section: Tnf Gene Variantsmentioning

confidence: 99%

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Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Grzela¹

2010

Mol Med Rep

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Abstract. Venous leg ulceration is a severe complication of chronic venous insufficiency. Despite numerous studies, understanding of the possible mechanisms involved in venous ulceration development remains incomplete. It is assumed that, in addition to well-documented behavioral and/or environmental conditions, as yet poorly defined genetic risk factors may play important roles in chronic wound progression or healing. It is difficult to overestimate the clinical usefulness of genetic screening in the determination of the risk of wound development and/or its healing course. From a pharmacogenomic perspective, genetic screening may aid in the planning of individualized treatment. In addition, the detection of venous ulcer-promoting gene variants may facilitate the decision to introduce prophylaxis or, if necessary, appropriate treatment for venous insufficiency, long before a leg ulcer develops. In addition to significant economic benefits, this approach would reduce the risk of health-and life-threatening conditions. In this review, we focus on several gene mutations/polymorphisms with previously documented significance in leg ulceration pathophysiology, and briefly speculate about possible candidates for further study.

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Section: Tnf Gene Variantsmentioning

confidence: 81%

Section: Tnf Gene Variantsmentioning

confidence: 99%

Section: Tnf Gene Variantsmentioning

confidence: 99%

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Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Grzela¹

2010

Mol Med Rep

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“…In RAU, the most common oral mucosal disease, the salivary levels of VEGF have been also associated with oral ulceration [52]. Finally, genetic variation in the VEGF gene has been also associated with the risk of developing gastroduodenal ulcers [53]. Evidence from these studies implicates angiogenesis in the pathophysiological development of oral ulcers, at both the genetic and at the functional level.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide pathway analysis identifies VEGF pathway association with oral ulceration in systemic lupus erythematosus

et al. 2017

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BackgroundSystemic lupus erythematosus (SLE) is a genetically complex rheumatic disease characterized by heterogeneous clinical manifestations of unknown etiology. Recent studies have suggested the existence of a genetic basis for SLE heterogeneity. The objective of the present study was to identify new genetic variation associated with the clinically relevant phenotypes in SLE.MethodsA two-stage pathway-based approach was used to identify the genetic variation associated with the main clinical phenotypes in SLE. In the discovery stage, 482 SLE patients were genotyped using Illumina Human Quad610 microarrays. Association between 798 reference genetic pathways from the Molecular Signatures Database and 11 SLE phenotypes was tested using the set-based method implemented in PLINK software. Pathways significantly associated after multiple test correction were subsequently tested for replication in an independent cohort of 425 SLE patients. Using an in silico approach, we analyzed the functional effects of common SLE therapies on the replicated genetic pathways. The association of known SLE risk variants with the development of the clinical phenotypes was also analyzed.ResultsIn the discovery stage, we found a significant association between the vascular endothelial growth factor (VEGF) pathway and oral ulceration (P value for false discovery rate (P FDR) < 0.05), and between the negative regulation signaling pathway of retinoic acid inducible gene-I/melanoma differentiation associated gene 5 and the production of antinuclear antibodies (P FDR < 0.05). In the replication stage, we validated the association between the VEGF pathway and oral ulceration. Therapies commonly used to treat mucocutaneous phenotypes in SLE were found to strongly influence VEGF pathway gene expression (P = 4.60e-4 to 5.38e-14). Analysis of known SLE risk loci identified a strong association between PTPN22 and the risk of hematologic disorder and with the development of antinuclear antibodies.ConclusionsThe present study has identified VEGF genetic pathway association with the risk of oral ulceration in SLE. New therapies targeting the VEGF pathway could be more effective in reducing the severity of this phenotype. These findings represent a first step towards the understanding of the genetic basis of phenotype heterogeneity in SLE.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-017-1345-6) contains supplementary material, which is available to authorized users.

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“…Kim et al. evaluated whether the vascular endothelial growth factor (VEGF) polymorphism could predict susceptibility to PUD through modified angiogenic activities and found that the VEGF polymorphism ‐ 1780T/C could significantly predict the predisposition to PUD after exposure to etiologic risks [12]. To understand the importance of this polymorphism, previously reported SNPs, such as IL‐1β and TNF‐α, are needed for a comparative study.…”

Section: Gastroduodenal Ulcer and H Pylori Infectionmentioning

confidence: 99%

Helicobacter pylori and Non‐malignant Diseases

Furuta

Delchier

2009

Helicobacter

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It is well known that Helicobacter pylori infection is associated with many nonmalignant disorders such as gastritis, peptic ulcer, gastroesophageal reflux disease (GERD), gastric polyp, nonsteroidal anti-inflammatory drug (NSAID)/aspirin-induced gastric injury, and functional dyspepsia. In 2008, interesting articles on the association of H. pylori infection with these disorders were presented, some of which intended to reveal the mechanisms of inter-individual differences in response to H. pylori infection, and have demonstrated that genetic differences in host and bacterial factors as well as environmental factors account for these differences. A decline in the occurrence of peptic ulcer related to H. pylori was confirmed. An inverse relationship between H. pylori infection and GERD was also confirmed but the impact of gastric atrophy on the prevention of GERD remained debatable. For NSAID-induced gastric injury, eradication of H. pylori infection has been recommended. During this year, eradication of H. pylori infection was recommended for patients treated with antiplatelet therapy as well as aspirin and NSAID. It was also reported that for patients with functional dyspepsia, eradication of H. pylori offers a modest but significant benefit.

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Novel single nucleotide polymorphism of the VEGF gene as a risk predictor for gastroduodenal ulcers

Abstract: The novel VEGF polymorphism -1780T/C could significantly predict the predisposition to GDU after the exposure to etiologic risks, based on defective angiogenic activity.

Cited by 10 publications

References 49 publications

Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Genome-wide pathway analysis identifies VEGF pathway association with oral ulceration in systemic lupus erythematosus

Helicobacter pylori and Non‐malignant Diseases

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