| pubmed-article:20491788 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C0003873 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C0224522 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C1421876 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C1441547 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C1264633 | lld:lifeskim |
| pubmed-article:20491788 | lifeskim:mentions | umls-concept:C1512167 | lld:lifeskim |
| pubmed-article:20491788 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:20491788 | pubmed:dateCreated | 2010-7-14 | lld:pubmed |
| pubmed-article:20491788 | pubmed:abstractText | Main features of rheumatoid arthritis (RA), hyperplasia of fibroblast-like synoviocytes (FLS) and joint destruction are caused by inflammatory cytokines produced in chronic autoimmune inflammation. Cell-intrinsic acquisition of tumour-like phenotypes of RA-FLS could also be responsible for the aggressive proliferation and invasion, which are supported by the fact that in some cases RA-FLS has mutations of a tumour suppressor gene TP53. However, the underlying molecular mechanism for TP53 mutations in RA-FLS has not yet been clarified. Recently it has been reported that the non-lymphoid cells in the inflammatory tissues express ectopically the activation-induced cytidine deaminase (AID) gene that induces somatic hypermutations, not only at the immunoglobulin (Ig) gene variable regions in germinal centre B lymphocytes but also at coding regions in TP53. Real-time polymerase chain reaction (PCR) analyses revealed more than half (five of nine) of the RA-FLS lines we established showed the markedly increased expression of AID. AID transcription in RA-FLS was augmented by tumour necrosis factor (TNF)-alpha and even by physiological concentration of beta-oestradiol that could not induce AID transcription in osteoarthritis-FLS. Furthermore, AID-positive RA-FLS presented a higher frequency of somatic mutations in TP53. Cytological and immunohistochemical analyses demonstrated clearly the ectopic expression of AID in the FLS at the RA synovium. These data suggested strongly a novel consequence of RA; the ectopic expression of AID in RA-FLS causes the somatic mutations and dysfunction of TP53, leading to acquisition of tumour-like properties by RA-FLS. | lld:pubmed |
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| pubmed-article:20491788 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20491788 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20491788 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20491788 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20491788 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:20491788 | pubmed:issn | 1365-2249 | lld:pubmed |
| pubmed-article:20491788 | pubmed:author | pubmed-author:TomitaTT | lld:pubmed |
| pubmed-article:20491788 | pubmed:author | pubmed-author:YoshikawaHH | lld:pubmed |
| pubmed-article:20491788 | pubmed:author | pubmed-author:IgarashiHH | lld:pubmed |
| pubmed-article:20491788 | pubmed:author | pubmed-author:HashimotoJJ | lld:pubmed |
| pubmed-article:20491788 | pubmed:author | pubmed-author:IshiharaKK | lld:pubmed |
| pubmed-article:20491788 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20491788 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:20491788 | pubmed:volume | 161 | lld:pubmed |
| pubmed-article:20491788 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20491788 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20491788 | pubmed:pagination | 71-80 | lld:pubmed |
| pubmed-article:20491788 | pubmed:dateRevised | 2011-8-1 | lld:pubmed |
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| pubmed-article:20491788 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20491788 | pubmed:articleTitle | TP53 mutations coincide with the ectopic expression of activation-induced cytidine deaminase in the fibroblast-like synoviocytes derived from a fraction of patients with rheumatoid arthritis. | lld:pubmed |
