Document Detail


Thioredoxin may exert a protective effect against tissue damage caused by oxidative stress in salivary glands of patients with Sjögren's syndrome.
MedLine Citation:
PMID:  17896802     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To demonstrate the existence of oxidative stress and the role of the antioxidant thioredoxin (TRX) in Sjögren's syndrome (SS). METHODS: Labial biopsy specimens from patients with SS were analyzed immunohistochemically to detect 8-hydroxy-2'-deoxyguanosine (8-OHdG), 4-hydroxy-2-nonenal (4-HNE), nitrotyrosine, and TRX. Levels of TRX in saliva and plasma were quantified by ELISA. To analyze the effect of TRX on human salivary gland (HSG) cells, recombinant TRX (rTRX)-treated HSG cells were stimulated by interferon-gamma (IFN-gamma) for detecting interleukin 6 (IL-6) with ELISA and RT-PCR, or stimulated with IFN-gamma and anti-Fas antibody for analyzing Fas-induced apoptosis with PI/annexin V staining. RESULTS: Large amounts of 8-OHdG, 4-HNE, nitrotyrosine, and TRX were produced in salivary duct cells of SS patients, whether there was periductal lymphocytic infiltration or not. Strong TRX expression was detected in acinar cells from 13 of 19 SS specimens. Levels of salivary TRX were significantly higher in SS patients than in controls (p < 0.05), and were inversely related to the salivary flow rates in SS patients. Patients who showed acinar TRX expression had higher salivary TRX levels than those who did not (p < 0.05). Interferon-gamma-induced expression of IL-6 and Fas-mediated apoptosis in HSG cells were significantly suppressed by pretreating cells with rTRX. CONCLUSION: Parallel production of oxidative stress markers together with massive secretion of TRX suggests that oxidative stress induces TRX in the salivary gland. Moreover, suppression of IL-6 production and apoptosis by rTRX in HSG cells suggests TRX acts to protect the salivary glands of SS patients from tissue damage.
Authors:
Chiyo Kurimoto; Seiji Kawano; Goh Tsuji; Saori Hatachi; Takumi Jikimoto; Daisuke Sugiyama; Shimpei Kasagi; Takahide Komori; Hajime Nakamura; Junji Yodoi; Shunichi Kumagai
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-09-15
Journal Detail:
Title:  The Journal of rheumatology     Volume:  34     ISSN:  0315-162X     ISO Abbreviation:  J. Rheumatol.     Publication Date:  2007 Oct 
Date Detail:
Created Date:  2007-10-10     Completed Date:  2008-02-25     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7501984     Medline TA:  J Rheumatol     Country:  Canada    
Other Details:
Languages:  eng     Pagination:  2035-43     Citation Subset:  IM    
Affiliation:
Department of Clinical Pathology and Immunology, Kobe University Graduate School of Medicine, Kobe, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Aldehydes / metabolism
Antioxidants / metabolism*
Apoptosis / physiology
Biological Markers / metabolism
Cysteine Proteinase Inhibitors / metabolism
Deoxyguanosine / analogs & derivatives,  metabolism
Female
Humans
Hydrogen Peroxide / metabolism
Interferon-gamma / metabolism
Interleukin-6 / genetics,  metabolism
Middle Aged
Oxidants / metabolism
Oxidative Stress*
Saliva / chemistry
Salivary Glands* / cytology,  metabolism,  pathology
Sjogren's Syndrome* / metabolism,  pathology
Thioredoxins / genetics,  metabolism*
Tyrosine / analogs & derivatives,  metabolism
Chemical
Reg. No./Substance:
0/8-hydroxy-2'-deoxyguanosine; 0/Aldehydes; 0/Antioxidants; 0/Biological Markers; 0/Cysteine Proteinase Inhibitors; 0/Interleukin-6; 0/Oxidants; 29343-52-0/4-hydroxy-2-nonenal; 3604-79-3/3-nitrotyrosine; 52500-60-4/Thioredoxins; 55520-40-6/Tyrosine; 7722-84-1/Hydrogen Peroxide; 82115-62-6/Interferon-gamma; 961-07-9/Deoxyguanosine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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