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      Toll-like Receptor 4 gene polymorphisms do not associate with normal tension glaucoma in a Korean population

      research-article
      Author(s): 1 , 1 , 2 , 1 ,
      Publication date (Electronic):
      Journal: Molecular Vision
      Publisher: Molecular Vision

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          Abstract

          Purpose

          To evaluate the association of Toll-like receptor 4 ( TLR4) gene polymorphisms with normal tension glaucoma (NTG) in the South Korean population.

          Methods

          A total of 147 normal tension glaucoma patients in South Korea were recruited from April, 2007 to August, 2008. Allele, genotype, and haplotype of 8 different types of TLR4 single nucleotide polymorphisms were analyzed: rs10759930, rs1927914, rs1927911, rs12377632, rs2149356, rs11536889, rs7037117, and rs7045953. Three hundred eighty healthy, unrelated South Korean adults were enrolled as controls.

          Results

          Frequencies of the TLR4 allele did not show any statistically significant difference between normal tension glaucoma patients and the control group (p>0.00625). The same results were observed in genotype frequency analysis. In addition, no statistically significant difference was observed in the frequency of haplotypes in cases of normal tension glaucoma when compared with controls.

          Conclusions

          TLR4 single nucleotide polymorphisms are not associated with normal tension glaucoma. Findings from this study suggest that TLR4 polymorphisms may not play an important role in NTG pathogenesis in the South Korean population.

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          Most cited references12

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          Toll-like receptors: critical proteins linking innate and acquired immunity.

          S Akira, K Takeda, T Kaisho (2001)
          Recognition of pathogens is mediated by a set of germline-encoded receptors that are referred to as pattern-recognition receptors (PRRs). These receptors recognize conserved molecular patterns (pathogen-associated molecular patterns), which are shared by large groups of microorganisms. Toll-like receptors (TLRs) function as the PRRs in mammals and play an essential role in the recognition of microbial components. The TLRs may also recognize endogenous ligands induced during the inflammatory response. Similar cytoplasmic domains allow TLRs to use the same signaling molecules used by the interleukin 1 receptors (IL-1Rs): these include MyD88, IL-1R--associated protein kinase and tumor necrosis factor receptor--activated factor 6. However, evidence is accumulating that the signaling pathways associated with each TLR are not identical and may, therefore, result in different biological responses.
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            Adult-onset primary open-angle glaucoma caused by mutations in optineurin.

            Tayebeh Rezaie, Anne Child, Roger Hitchings … (2002)
            Primary open-angle glaucoma (POAG) affects 33 million individuals worldwide and is a leading cause of blindness. In a study of 54 families with autosomal dominantly inherited adult-onset POAG, we identified the causative gene on chromosome 10p14 and designated it OPTN (for "optineurin"). Sequence alterations in OPTN were found in 16.7% of families with hereditary POAG, including individuals with normal intraocular pressure. The OPTN gene codes for a conserved 66-kilodalton protein of unknown function that has been implicated in the tumor necrosis factor-alpha signaling pathway and that interacts with diverse proteins including Huntingtin, Ras-associated protein RAB8, and transcription factor IIIA. Optineurin is expressed in trabecular meshwork, nonpigmented ciliary epithelium, retina, and brain, and we speculate that it plays a neuroprotective role.
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              Toll-like receptor 4 polymorphisms and atherogenesis.

              Johann Willeit, Eva Lorenz, Friedrich Oberhollenzer … (2002)
              The ability to mount a prominent inflammatory response to bacterial pathogens confers an advantage in innate immune defense but may signal an increased risk of atherosclerosis. We determined whether recently discovered genetic variants of toll-like receptor 4 (TLR4) that confer differences in the inflammatory response elicited by bacterial lipopolysaccharide are related to the development of atherosclerosis. As part of the five-year follow-up in the Bruneck (Italy) Study, we screened 810 persons in the study cohort for the TLR4 polymorphisms Asp299Gly and Thr399Ile. The extent and progression of carotid atherosclerosis were assessed by high-resolution duplex ultrasonography. As compared with subjects with wild-type TLR4, the 55 subjects with the Asp299Gly TLR4 allele had lower levels of certain proinflammatory cytokines, acute-phase reactants, and soluble adhesion molecules, such as interleukin-6 and fibrinogen. Although these subjects were found to be more susceptible to severe bacterial infections, they had a lower risk of carotid atherosclerosis (odds ratio, 0.54; 95 percent confidence interval, 0.32 to 0.98; P=0.05) and a smaller intima-media thickness in the common carotid artery (regression coefficient, -0.07; 95 percent confidence interval, -0.12 to -0.02; P=0.01). The Asp299Gly TLR4 polymorphism, which attenuates receptor signaling and diminishes the inflammatory response to gram-negative pathogens, is associated with a decreased risk of atherosclerosis. This finding is consistent with the hypothesis that innate immunity may play a part in atherogenesis. Copyright 2002 Massachusetts Medical Society.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Vis
                Journal ID (publisher-id): MV
                Title: Molecular Vision
                Publisher: Molecular Vision
                ISSN (Electronic): 1090-0535
                Publication date Collection: 2011
                Publication date (Electronic): 31 August 2011
                Volume: 17
                Pages: 2343-2348
                Affiliations
                [1 ]Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
                [2 ]Department of Laboratory Medicine & Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
                Author notes
                Correspondence to: Changwon Kee, M.D., Ph.D., Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine 50 Ilwon-dong, Gangnam-gu, Seoul, 135-710, Republic of Korea; Phone: 82-2-3410-3564; FAX: 82-2-3410-0074; email: ckee@ 123456skku.edu
                Article
                Publisher ID: 255 Publisher ID: 2011MOLVIS0278
                PMC ID: 3171501
                PubMed ID: 21921986
                SO-VID: 4d6a13cc-d148-46a4-a6f3-ea9e92bf93e4
                Copyright © Copyright © 2011 Molecular Vision.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 09 May 2011
                Date accepted : 25 August 2011
                Categories
                Subject: Research Article
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                corr-author Kee

                ScienceOpen disciplines: Vision sciences
                Data availability:
                ScienceOpen disciplines: Vision sciences

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