| Altered ganglioside expression modulates the pathogenic mechanism of thyroid-associated ophthalmopathy by increase in hyaluronic acid. | |
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MedLine Citation:
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PMID: 20811057 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: The aim of this study was to determine the role of gangliosides in pathogenic mechanisms of thyroid-associated ophthalmopathy (TAO). METHODS: The gangliosides profile and mRNA level of sialyltransferases of the orbital tissues from TAO patients (n = 5) and non-TAO subjects (n = 4) were investigated. In addition, the effect of exogenous gangliosides on the expression of hyaluronic acid was examined in orbital fibroblasts. For in vitro experiments, we used four different strains of cells obtained from non-TAO subjects with at least three replicates for each strain. RESULTS: Trisialoganglioside 1b (GT1b) was significantly overexpressed in the orbital tissue of TAO patients compared with control tissue, whereas no significant difference was observed for either monosialoganglioside 1 (GM1) or disialoganglioside 1a (GD1a) by digital analyses of immunohistochemical images. Moreover, mRNA levels of sialyltransferase (SAT)-I and SAT II were increased in TAO patients compared with control. Exogenous GT1b strongly induced the morphologic changes related to an accumulation of sparse flocculent precipitates in lysosomes and increased the extracellular hyaluronic acid level in orbital fibroblasts with the induction of hyaluronic acid synthase, which were less by GD1a but not by GM1. The GT1b-induced morphologic changes of cells were due, at least in part, to an increase of intracellular hyaluronic acid. Co-treatment of hyaluronidase nicely attenuated the morphologic changes in orbital fibroblasts. Thy-1(+) orbital fibroblasts were more capable of producing hyaluronic acid by exogenous GT1b. CONCLUSIONS: The results suggest that gangliosides, particularly GT1b, may play a role in the pathologic mechanisms of TAO by stimulating an increase in hyaluronic acid. |
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Authors:
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Koung Hoon Kook; Youn-Hee Choi; Yu Rim Kim; Soo Jung Park; Ilo Jou; Sung Joo Kim; Sang Yeul Lee |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-01-05 |
Journal Detail:
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Title: Investigative ophthalmology & visual science Volume: 52 ISSN: 1552-5783 ISO Abbreviation: Invest. Ophthalmol. Vis. Sci. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-01-06 Completed Date: 2011-02-07 Revised Date: 2011-03-04 |
Medline Journal Info:
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Nlm Unique ID: 7703701 Medline TA: Invest Ophthalmol Vis Sci Country: United States |
Other Details:
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Languages: eng Pagination: 264-73 Citation Subset: IM |
Affiliation:
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Department of Ophthalmology, Ajou University School of Medicine,Yeongtong-gu, Suwon 443-721, Korea. drkook@ajou.ac.kr |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Antigens, CD / genetics Cells, Cultured Enzyme-Linked Immunosorbent Assay Female Fibroblasts / metabolism Fluorescent Antibody Technique, Indirect G(M1) Ganglioside / physiology Gangliosides / physiology* Graves Ophthalmopathy / etiology*, metabolism Humans Hyaluronic Acid / metabolism* Male Middle Aged Orbit / metabolism, pathology RNA, Messenger / genetics Reverse Transcriptase Polymerase Chain Reaction Sialyltransferases / genetics |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD; 0/Gangliosides; 0/RNA, Messenger; 0/sialogangliosides; 37758-47-7/G(M1) Ganglioside; 59247-13-1/trisialoganglioside GT1; 9004-61-9/Hyaluronic Acid; EC 2.4.99.-/Sialyltransferases; EC 2.4.99.1/ST6GAL1 protein, human; EC 2.4.99.8/alpha-N-acetylneuraminate alpha-2,8-sialyltransferase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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