Document Detail


The role of C1GALT1C1 in lipopolysaccharide-induced IgA1 aberrant O-glycosylation in IgA nephropathy.
MedLine Citation:
PMID:  20144270     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: IgA1 aberrant O-glycosylation is one of the main pathogenetic features of IgA nephropathy (IgAN). This study attempted to determine the role of C1GALT1C1 in aberrant IgA1 O-glycosylation induced by lipopolysaccharide (LPS) and identify potential therapeutic targets in IgAN. METHODS: Lymphocytes isolated from 22 patients with IgAN and 17 normal controls were cultured for 3 to 7 days with or without LPS and 5-azacytidine (5-AZA). Expression levels of C1GALT1C1 mRNA and protein were measured by real-time PCR and Western blot analysis, respectively. Concentration of IgA1 and level of O-glycosylation were determined by ELISA and Vicia villosa (VV) lectin-binding assay. Correlation analysis was performed between the expression of C1GALT1C1 protein and IgA1 O-glycosylation. RESULTS: Lymphocytes from patients with IgAN secreted more IgA1 than that from normal controls after LPS stimulation (P=0.26, 0.002 and 0.005 on the 3rd, 5th and 7th day, respectively) which could be inhibited by 5-AZA (P=0.001, 0.025 and 0.001 on the 3rd, 5th and 7th day, respectively). Moreover, LPS stimulation could obviously inhibit C1GALT1C1 expression in patients with IgAN (decreased by 71%, 82% and 92% on the 3rd, 5th and 7th day, respectively; P < 0.001), and cause a significant decrease of IgA1 O-glycosylation compared with normal controls (P=0.004, 0.003 and 0.03 on the 3rd, 5th and 7th day, respectively). When 5-AZA was added, the level of C1GALT1C1 expression increased dramatically (1.98, 5.53 and 8.97 times on the 3rd, 5th and 7th day, respectively; P < 0.001) along with an increase of IgA1 O-glycosylation (P=0.295, 0.09 and 0.003 on the 3rd, 5th and 7th day, respectively). However, normal controls showed no significant change in C1GALT1C1 expression and IgA1 O-glycosylation after LPS stimulation (P > 0.05). CONCLUSION: LPS induced IgA1 aberrant O-glycosylation and suppressed C1GALT1C1 expression in patients with IgAN. Upregulation of C1GALT1C1 expression by 5-AZA could reverse the IgA1 aberrant O-glycosylation. These results suggest that C1GALT1C1 may play a key role in the regulation of IgA1 O-glycosylation.
Authors:
Lin-Shen Xie; Wei Qin; Jun-Ming Fan; Jun Huang; Xi-Sheng Xie; Zi Li
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-01
Journal Detail:
Title:  Clinical and investigative medicine. M?decine clinique et experimentale     Volume:  33     ISSN:  1488-2353     ISO Abbreviation:  Clin Invest Med     Publication Date:  2010  
Date Detail:
Created Date:  2010-02-10     Completed Date:  2010-04-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7804071     Medline TA:  Clin Invest Med     Country:  Canada    
Other Details:
Languages:  eng     Pagination:  E5-13     Citation Subset:  IM    
Affiliation:
Department of Nephrology, West China Hospital of Sichuan University, Chengdu City, Sichuan Province, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Azacitidine / metabolism
Case-Control Studies
Cells, Cultured
Female
Glomerulonephritis, IGA / immunology*,  metabolism
Glycosylation
Humans
Immunoglobulin A / immunology*,  metabolism
Lipopolysaccharides / metabolism
Lymphocytes / metabolism
Male
Molecular Chaperones / genetics,  metabolism*
RNA, Messenger / metabolism
Time Factors
Up-Regulation / immunology
Young Adult
Chemical
Reg. No./Substance:
0/C1GALT1C1 protein, human; 0/Immunoglobulin A; 0/Lipopolysaccharides; 0/Molecular Chaperones; 0/RNA, Messenger; 320-67-2/Azacitidine

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


Previous Document:  CD133+ human pulmonary adenocarcinoma cells induce apoptosis of CD8+T cells by highly expressed gale...
Next Document:  Comparison of two oscillometric blood pressure monitors in subjects with atrial fibrillation.