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Alterations of serum protein N-glycosylation in two mouse models of chronic liver disease are hepatocyte and not B cell driven

BRAM BLOMME UGent, Christophe Van Steenkiste UGent, Paola Grassi, Stuart M Haslam, Anne Dell, Nico Callewaert UGent and Hans Van Vlierberghe UGent (2011) AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY. 300(5). p.G833-G842
abstract
N-glycosylation of immunoglobulin G (IgG) has an important impact on the modification of the total serum N-glycome in chronic liver patients. Our aim was to determine the role and magnitude of the alterations in which hepatocytes and B cells are involved in two mouse models of chronic liver disease. Common bile duct ligation (CBDL) and subcutaneous injections with CCl(4) were induced in B cell-deficient and wild-type (WT) mice. IgG depletion was performed with beads covered with protein A/G and the depletions were evaluated by SDS-PAGE and Western blot analysis. N-glycan analysis was performed by improved DSA-FACE technology. Structural analysis of the mouse serum N-glycans was performed by exoglycosidase digests and MALDI-TOF mass spectrometry of permethylated glycans. The alterations seen in B cell-deficient mice closely resembled the alterations in WT mice, in both the CBDL and the CCl(4) models. N-glycan analysis of the IgG fraction in both mouse models revealed different changes compared with humans. Overall, the impact of IgG glycosylation on total serum glycosylation was marginal. Interestingly, the amount of fibrosis present in CBDL B cell-deficient mice was significantly increased compared with CBDL WT mice, whereas the opposite was true for the CCl(4) model as determined by Sirius red staining. However, this had no major effect on the alteration of N-glycosylation of serum proteins. Alterations of total serum N-glycome in mouse models of chronic liver disease are hepatocyte-driven. Undergalactosylation of IgG is not present in mouse models of chronic liver disease.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
GLYCANS, GLYCOME, FIBROSIS, GALACTOSYLATION, CIRRHOSIS, SUGAR CHAINS, IMMUNOGLOBULIN-G, HEPATOCELLULAR-CARCINOMA PATIENTS, CBDL, DSA-FACE, MICE, GLYCOPROTEINS, CCl4, glycomics, B cells
journal title
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
Am. J. Physiol.-Gastroint. Liver Physiol.
volume
300
issue
5
pages
G833 - G842
Web of Science type
Article
Web of Science id
000289938700018
JCR category
GASTROENTEROLOGY & HEPATOLOGY
JCR impact factor
3.431 (2011)
JCR rank
18/73 (2011)
JCR quartile
1 (2011)
ISSN
0193-1857
DOI
10.1152/ajpgi.00228.2010
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1222702
handle
http://hdl.handle.net/1854/LU-1222702
date created
2011-05-13 09:24:12
date last changed
2015-06-17 09:33:50
@article{1222702,
  abstract     = {N-glycosylation of immunoglobulin G (IgG) has an important impact on the modification of the total serum N-glycome in chronic liver patients. Our aim was to determine the role and magnitude of the alterations in which hepatocytes and B cells are involved in two mouse models of chronic liver disease. Common bile duct ligation (CBDL) and subcutaneous injections with CCl(4) were induced in B cell-deficient and wild-type (WT) mice. IgG depletion was performed with beads covered with protein A/G and the depletions were evaluated by SDS-PAGE and Western blot analysis. N-glycan analysis was performed by improved DSA-FACE technology. Structural analysis of the mouse serum N-glycans was performed by exoglycosidase digests and MALDI-TOF mass spectrometry of permethylated glycans. The alterations seen in B cell-deficient mice closely resembled the alterations in WT mice, in both the CBDL and the CCl(4) models. N-glycan analysis of the IgG fraction in both mouse models revealed different changes compared with humans. Overall, the impact of IgG glycosylation on total serum glycosylation was marginal. Interestingly, the amount of fibrosis present in CBDL B cell-deficient mice was significantly increased compared with CBDL WT mice, whereas the opposite was true for the CCl(4) model as determined by Sirius red staining. However, this had no major effect on the alteration of N-glycosylation of serum proteins. Alterations of total serum N-glycome in mouse models of chronic liver disease are hepatocyte-driven. Undergalactosylation of IgG is not present in mouse models of chronic liver disease.},
  author       = {BLOMME, BRAM and Van Steenkiste, Christophe and Grassi, Paola and Haslam, Stuart M and Dell, Anne and Callewaert, Nico and Van Vlierberghe, Hans},
  issn         = {0193-1857},
  journal      = {AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY},
  keyword      = {GLYCANS,GLYCOME,FIBROSIS,GALACTOSYLATION,CIRRHOSIS,SUGAR CHAINS,IMMUNOGLOBULIN-G,HEPATOCELLULAR-CARCINOMA PATIENTS,CBDL,DSA-FACE,MICE,GLYCOPROTEINS,CCl4,glycomics,B cells},
  language     = {eng},
  number       = {5},
  pages        = {G833--G842},
  title        = {Alterations of serum protein N-glycosylation in two mouse models of chronic liver disease are hepatocyte and not B cell driven},
  url          = {http://dx.doi.org/10.1152/ajpgi.00228.2010},
  volume       = {300},
  year         = {2011},
}

Chicago
BLOMME, BRAM, Christophe Van Steenkiste, Paola Grassi, Stuart M Haslam, Anne Dell, Nico Callewaert, and Hans Van Vlierberghe. 2011. “Alterations of Serum Protein N-glycosylation in Two Mouse Models of Chronic Liver Disease Are Hepatocyte and Not B Cell Driven.” American Journal of Physiology-gastrointestinal and Liver Physiology 300 (5): G833–G842.
APA
BLOMME, BRAM, Van Steenkiste, C., Grassi, P., Haslam, S. M., Dell, A., Callewaert, N., & Van Vlierberghe, H. (2011). Alterations of serum protein N-glycosylation in two mouse models of chronic liver disease are hepatocyte and not B cell driven. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 300(5), G833–G842.
Vancouver
1.
BLOMME B, Van Steenkiste C, Grassi P, Haslam SM, Dell A, Callewaert N, et al. Alterations of serum protein N-glycosylation in two mouse models of chronic liver disease are hepatocyte and not B cell driven. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY. 2011;300(5):G833–G842.
MLA
BLOMME, BRAM, Christophe Van Steenkiste, Paola Grassi, et al. “Alterations of Serum Protein N-glycosylation in Two Mouse Models of Chronic Liver Disease Are Hepatocyte and Not B Cell Driven.” AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY 300.5 (2011): G833–G842. Print.