GATA3 siRNA inhibits the binding of NFAT1 to interleukin-13 promoter in human T cells / 中华医学杂志(英文版)
Chinese Medical Journal
; (24): 739-744, 2010.
Article
in En
| WPRIM
| ID: wpr-242579
Responsible library:
WPRO
ABSTRACT
<p><b>BACKGROUND</b>Interleukin-13 (IL-13) is recognized to be a key modulator in the pathogenesis of Th2-induced allergic inflammation. Transcription factors GATA3 and NFAT1 have been both implicated in the regulation of Th2 cytokines. We previously demonstrated the GATA3-NFAT1 association during human T cell activation. However, the function of the GATA3-NFAT1 complex in Th2 cytokines regulation is still unknown. Small interference RNA (siRNA) was constructed to knock down GATA3 expression in Hut-78 cells to investigate the possible role of GATA3-NFAT1 complex in IL-13 transcription.</p><p><b>METHODS</b>Cells were stimulated with anti-CD3 plus anti-CD28 antibodies to mimic in vivo antigen-mediated co-stimulation; the expression of IL-13 mRNA was determined by real-time PCR; chromation immunoprecipitation (CHIP) assay was employed to investigate the NFAT1 binding to IL-13 promoter.</p><p><b>RESULTS</b>GATA3 siRNA suppressed the expression of GATA3 both in mRNA and protein levels in Hut-78 cells. The binding of NFAT1 to IL-13 promoter was inhibited by GATA3 siRNA in activated T cells, which was followed by the reduction of IL-13 transcription.</p><p><b>CONCLUSION</b>GATA3-NFAT1 complex may play an important role in the regulation of IL-13 transcription in human T cells.</p>
Full text:
1
Index:
WPRIM
Main subject:
T-Lymphocytes
/
Transfection
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Cells, Cultured
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Promoter Regions, Genetic
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Interleukin-13
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RNA, Small Interfering
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GATA3 Transcription Factor
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NFATC Transcription Factors
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Genetics
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Metabolism
Limits:
Humans
Language:
En
Journal:
Chinese Medical Journal
Year:
2010
Type:
Article