PMID- 7959594
OWN - NLM
STAT- MEDLINE
DCOM- 19941228
LR  - 20061115
IS  - 0367-6102 (Print)
IS  - 0367-6102 (Linking)
VI  - 69
IP  - 4
DP  - 1994 Jul
TI  - [Expression of human endogenous retroviruses in rheumatoid arthritis].
PG  - 821-35
AB  - The genomes of all organisms, from yeast to humans, contain thousands of 
      endogenous retroviruses (ERVs) and ERVs are transmitted vertically through germ 
      cells as provirus. In recent studies, it has been reported that some ERVs have 
      important immunologic effects and are associated with autoimmune diseases in 
      several animals. However, despite many years of investigation in human, 
      physiological or pathological roles for ERVs remain unknown. In this study we 
      examined whether the pathogenesis of rheumatoid arthritis (RA) was associated 
      with human ERVs; ERV3 and lambda 4-1, which retain open reading frames (ORF) and 
      could make proteins. We demonstrated that ERV3 and lambda 4-1 were expressed on 
      synoviocytes and peripheral blood mononuclear cells (PBMCs) in RA patients by 
      Northern blot analysis. But the expression was indeed heterogenous: RA patients 
      showed various expression levels of ERV3 and lambda 4-1, which were independent 
      of clinical activities and kinds of used drugs. mRNAs of ERV3 and lambda 4-1 were 
      also expressed in PBMCs of healthy volunteers. We detected a 4.2 kb transcript of 
      lambda 4-1 in synoviocytes and PBMCs which was not expressed in placentas, 
      suggesting a unique protein might be produced in synoviocytes and PBMCs compared 
      to placentas. In order to examine regulatory mechanisms for expression of human 
      ERVs, we treated cultured synoviocytes and human kidney endothelial cells (hKEC) 
      with various cytokines. By interleukin-1 beta (IL-1 beta) treatment, ERV3 
      expression in synoviocytes was not altered, but that in hKEC increased and 
      correlated with IL-6 expression. Although ERV3 and lambda 4-1 expression may not 
      be directly associated with the pathogenesis of RA, the possibility still exists 
      that some of many ERVs, which are integrated into human genomes, may have 
      causative roles in RA.
FAU - Takeuchi, K
AU  - Takeuchi K
AD  - First Department of Pathology, Hokkaido University School of Medicine, Sapporo, 
      Japan.
LA  - jpn
PT  - English Abstract
PT  - Journal Article
PL  - Japan
TA  - Hokkaido Igaku Zasshi
JT  - [Hokkaido igaku zasshi] The Hokkaido journal of medical science
JID - 17410290R
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Viral)
SB  - IM
MH  - Animals
MH  - Arthritis, Rheumatoid/etiology/*virology
MH  - Cells, Cultured
MH  - Humans
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Restriction Fragment Length
MH  - RNA, Messenger/analysis
MH  - RNA, Viral/analysis
MH  - Retroviridae/*isolation & purification
MH  - Synovial Membrane/virology
EDAT- 1994/07/01 00:00
MHDA- 1994/07/01 00:01
CRDT- 1994/07/01 00:00
PHST- 1994/07/01 00:00 [pubmed]
PHST- 1994/07/01 00:01 [medline]
PHST- 1994/07/01 00:00 [entrez]
PST - ppublish
SO  - Hokkaido Igaku Zasshi. 1994 Jul;69(4):821-35.