BROWSE

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Author

Kwon, H. Moo
Inflammation and Kidney Disorder Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorders, Genomic instability

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NF-AT5 Is a Critical Regulator of Inflammatory Arthritis

Cited 10 times inthomson ciCited 11 times inthomson ci
Title
NF-AT5 Is a Critical Regulator of Inflammatory Arthritis
Author
Yoon, Hyung-JuYou, SungyongYoo, Seung-AhKim, Nam-HoonKwon, H. MooYoon, Chong-HyeonCho, Chul-SooHwang, DaeheeKim, Wan-Uk
Keywords
ENHANCER-BINDING PROTEIN; T-CELL-ACTIVATION; RHEUMATOID-ARTHRITIS; GROWTH-FACTOR; SYNOVIAL FIBROBLASTS; HYPERTONIC STRESS; ANGIOGENESIS; TRANSCRIPTION; EXPRESSION; GENE
Issue Date
201107
Publisher
WILEY-BLACKWELL
Citation
ARTHRITIS AND RHEUMATISM, v.63, no.7, pp.1843 - 1852
Abstract
Objective. To investigate the role of NF-AT5, an osmoprotective transcription factor, in synovial hyperplasia and angiogenesis in patients with rheumatoid arthritis (RA). Methods. The expression of NF-AT5 in synovial tissue and synoviocytes from RA patients was examined by immunohistochemistry and Western blot analysis, respectively. Messenger RNA (mRNA) in RA synoviocytes and human umbilical vein endothelial cells (HUVECs) transfected with dummy small interfering RNA (siRNA) or NF-AT5 siRNA were profiled using microarray technology. Assays to determine synoviocyte apoptosis and proliferation were performed in the presence of NF-AT5 siRNA. VEGF(165)-induced angiogenesis was assessed by measuring the proliferation, tube formation, and wound migration of HUVECs. Experimental arthritis was induced in mice by injection of anti-type II collagen antibody. Results. NF-AT5 was highly expressed in rheumatoid synovium, and its activity was increased by proinflammatory cytokines, such as interleukin-1 beta and tumor necrosis factor alpha. The mRNA profiling of synoviocytes and HUVECs transfected with NF-AT5-targeted siRNA revealed 3 major changes in cellular processes associated with the pathogenesis of RA: cell cycle and survival, angiogenesis, and cell migration. Consistent with these results, NF-AT5 knockdown in RA synoviocytes and HUVECs inhibited their proliferation/survival and impeded angiogenic processes in HUVECs. Mice with NF-AT5 haploinsufficiency (NF-AT5(+/-)) developed a very limited degree of synovial proliferation, as seen on histologic analysis, and decreased angiogenesis, and they exhibited a nearly complete suppression of experimentally induced arthritis. Conclusion. NF-AT5 regulates synovial proliferation and angiogenesis in chronic arthritis.
URI
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DOI
http://dx.doi.org/10.1002/art.30229
ISSN
0004-3591
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