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Title: Role of galectin-3 in prion infections of the CNS

Abstract

Galectin-3 is a multi-functional protein and participates in mediating inflammatory reactions. The pronounced overexpression of galectin-3 in prion-infected brain tissue prompted us to study the role of this protein in a murine prion model. Immunofluorescence double-labelling identified microglia as the major cell type expressing galectin-3. Ablation of galectin-3 did not affect PrP{sup Sc}-deposition and development of gliosis. However, galectin-3{sup -/-}-mice showed prolonged survival times upon intracerebral and peripheral scrapie infections. Moreover, protein levels of the lysosomal activation marker LAMP-2 were markedly reduced in prion-infected galectin-3{sup -/-}-mice suggesting a role of galectin-3 in regulation of lysosomal functions. Lower mRNA levels of Beclin-1 and Atg5 in prion-infected wild-type and galectin-3{sup -/-}-mice indicated an impairment of autophagy although autophagosome formation was unchanged. The results point towards a detrimental role of galectin-3 in prion infections of the CNS and suggest that endo-/lysosomal dysfunction in combination with reduced autophagy may contribute to disease development.

Authors:
 [1];  [1];  [2];  [3];  [3];  [1];  [1];  [1]
  1. Project Neurodegenerative Diseases, Robert-Koch-Institut, Nordufer 20, 13353 Berlin (Germany)
  2. Center for Biological Safety 4, Robert-Koch-Institut, Nordufer 20, 13353 Berlin (Germany)
  3. Department of Dermatology, School of Medicine, University of California-Davis, Sacramento, CA 95817 (United States)
Publication Date:
OSTI Identifier:
20991472
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 359; Journal Issue: 3; Other Information: DOI: 10.1016/j.bbrc.2007.05.163; PII: S0006-291X(07)01140-0; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ABLATION; BRAIN; DEPOSITION; DOUBLE LABELLING; GENE REGULATION; INFLAMMATION; MICE; PROTEINS

Citation Formats

Mok, Simon W.F., Riemer, Constanze, Madela, Kazimierz, Hsu, Daniel K, Liu, Fu-Tong, Gueltner, Sandra, Heise, Ines, and Baier, Michael. Role of galectin-3 in prion infections of the CNS. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2007.05.163.
Mok, Simon W.F., Riemer, Constanze, Madela, Kazimierz, Hsu, Daniel K, Liu, Fu-Tong, Gueltner, Sandra, Heise, Ines, & Baier, Michael. Role of galectin-3 in prion infections of the CNS. United States. https://doi.org/10.1016/j.bbrc.2007.05.163
Mok, Simon W.F., Riemer, Constanze, Madela, Kazimierz, Hsu, Daniel K, Liu, Fu-Tong, Gueltner, Sandra, Heise, Ines, and Baier, Michael. 2007. "Role of galectin-3 in prion infections of the CNS". United States. https://doi.org/10.1016/j.bbrc.2007.05.163.
@article{osti_20991472,
title = {Role of galectin-3 in prion infections of the CNS},
author = {Mok, Simon W.F. and Riemer, Constanze and Madela, Kazimierz and Hsu, Daniel K and Liu, Fu-Tong and Gueltner, Sandra and Heise, Ines and Baier, Michael},
abstractNote = {Galectin-3 is a multi-functional protein and participates in mediating inflammatory reactions. The pronounced overexpression of galectin-3 in prion-infected brain tissue prompted us to study the role of this protein in a murine prion model. Immunofluorescence double-labelling identified microglia as the major cell type expressing galectin-3. Ablation of galectin-3 did not affect PrP{sup Sc}-deposition and development of gliosis. However, galectin-3{sup -/-}-mice showed prolonged survival times upon intracerebral and peripheral scrapie infections. Moreover, protein levels of the lysosomal activation marker LAMP-2 were markedly reduced in prion-infected galectin-3{sup -/-}-mice suggesting a role of galectin-3 in regulation of lysosomal functions. Lower mRNA levels of Beclin-1 and Atg5 in prion-infected wild-type and galectin-3{sup -/-}-mice indicated an impairment of autophagy although autophagosome formation was unchanged. The results point towards a detrimental role of galectin-3 in prion infections of the CNS and suggest that endo-/lysosomal dysfunction in combination with reduced autophagy may contribute to disease development.},
doi = {10.1016/j.bbrc.2007.05.163},
url = {https://www.osti.gov/biblio/20991472}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 3,
volume = 359,
place = {United States},
year = {Fri Aug 03 00:00:00 EDT 2007},
month = {Fri Aug 03 00:00:00 EDT 2007}
}