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Chronicity of pristane-induced arthritis in rats is controlled by genes on chromosome 14

Wester Rosenlöf, Lena LU ; Olofsson, Peter LU ; Ibrahim, SM and Holmdahl, Rikard LU (2003) In Journal of Autoimmunity 21(4). p.305-313
Abstract
To, address; he possibility, that genes specifically control the chronic phase of arthritis we have isolated a congenic fragment from the resistant E3; rat cm the, susceptible DA rat background. The isolated fragment covers the Pia6 quantitative trait locus on chromosome 14, which previously has been identified to be linked to chronic pristane induced arthritis (PIA) in gene segregation experiments; of an (E3 x DA) F-2-cross. Heterozygous. Pia6 congenic rats (DA.Pia6) were protected from chronic active arthritis specifically, as determined by macroscopic scoring, histopathology and release of cartilage oligomeric matrix protein (-reflecting ongoing cartilage destruction). The difference was seen only during the chronic active phase of... (More)
To, address; he possibility, that genes specifically control the chronic phase of arthritis we have isolated a congenic fragment from the resistant E3; rat cm the, susceptible DA rat background. The isolated fragment covers the Pia6 quantitative trait locus on chromosome 14, which previously has been identified to be linked to chronic pristane induced arthritis (PIA) in gene segregation experiments; of an (E3 x DA) F-2-cross. Heterozygous. Pia6 congenic rats (DA.Pia6) were protected from chronic active arthritis specifically, as determined by macroscopic scoring, histopathology and release of cartilage oligomeric matrix protein (-reflecting ongoing cartilage destruction). The difference was seen only during the chronic active phase of arthritis starting approximately 5 weeks after onset of arthritis. Interestingly, the plasma concentration of the lipocalins alpha(1)-acid glycoprotein and alpha(1)-microglobulin was found significantly altered in naive congenic rats compared to the DA rat. The concentration of alpha(1)-microglobulin was found to be significantly higher throughout the disease course, while alpha(1)-acid glycoprotein had a lower concentration in naive rats, which was highly significant in the chronic phase. The altered concentrations of these proteins already before development of chronic arthritis may provide a clue to the pathogenic process controlled by the Pia6 genes. We conclude that the active relapsing chronic arthritis is under a unique genetic control that is different from the control of acute arthritis and postulate that the liver plays an important role in this relagation. (C) 2003 Elsevier Ltd. All rights reserved.. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
liver, congenic animal, cartilage oligomeric matrix protein, alpha(1)-microglobulin, alpha(1)-acid glycoprotein
in
Journal of Autoimmunity
volume
21
issue
4
pages
305 - 313
publisher
Elsevier
external identifiers
  • pmid:14624754
  • wos:000186825200002
  • scopus:0242490252
ISSN
0896-8411
DOI
10.1016/S0896-8411(03)00136-7
language
English
LU publication?
yes
id
36d21b18-6e02-452b-b9b8-92ea5229d88b (old id 294468)
date added to LUP
2007-09-24 08:04:26
date last changed
2018-01-07 05:19:20
@article{36d21b18-6e02-452b-b9b8-92ea5229d88b,
  abstract     = {To, address; he possibility, that genes specifically control the chronic phase of arthritis we have isolated a congenic fragment from the resistant E3; rat cm the, susceptible DA rat background. The isolated fragment covers the Pia6 quantitative trait locus on chromosome 14, which previously has been identified to be linked to chronic pristane induced arthritis (PIA) in gene segregation experiments; of an (E3 x DA) F-2-cross. Heterozygous. Pia6 congenic rats (DA.Pia6) were protected from chronic active arthritis specifically, as determined by macroscopic scoring, histopathology and release of cartilage oligomeric matrix protein (-reflecting ongoing cartilage destruction). The difference was seen only during the chronic active phase of arthritis starting approximately 5 weeks after onset of arthritis. Interestingly, the plasma concentration of the lipocalins alpha(1)-acid glycoprotein and alpha(1)-microglobulin was found significantly altered in naive congenic rats compared to the DA rat. The concentration of alpha(1)-microglobulin was found to be significantly higher throughout the disease course, while alpha(1)-acid glycoprotein had a lower concentration in naive rats, which was highly significant in the chronic phase. The altered concentrations of these proteins already before development of chronic arthritis may provide a clue to the pathogenic process controlled by the Pia6 genes. We conclude that the active relapsing chronic arthritis is under a unique genetic control that is different from the control of acute arthritis and postulate that the liver plays an important role in this relagation. (C) 2003 Elsevier Ltd. All rights reserved..},
  author       = {Wester Rosenlöf, Lena and Olofsson, Peter and Ibrahim, SM and Holmdahl, Rikard},
  issn         = {0896-8411},
  keyword      = {liver,congenic animal,cartilage oligomeric matrix protein,alpha(1)-microglobulin,alpha(1)-acid glycoprotein},
  language     = {eng},
  number       = {4},
  pages        = {305--313},
  publisher    = {Elsevier},
  series       = {Journal of Autoimmunity},
  title        = {Chronicity of pristane-induced arthritis in rats is controlled by genes on chromosome 14},
  url          = {http://dx.doi.org/10.1016/S0896-8411(03)00136-7},
  volume       = {21},
  year         = {2003},
}