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Published on: December 4, 2018
Basic-helix-loop-helix transcription factor DEC2 constitutes negative feedback loop in IFN-β-mediated inflammatory
Tadaatsu Imaizumi1, Fuyuki Sato, Hiroshi Tanaka
1Department of Vascular Biology, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan. timaizum@cc.hirosaki-u.ac.jp
Immunology Letters
|December 7, 2010
Summary
Differentiated embryo-chondrocyte 2 (DEC2) regulates kidney inflammation. Its expression, triggered by double-stranded RNA, acts as a negative feedback mechanism for inflammatory responses in human mesangial cells.
Area of Science:
- Immunology
- Molecular Biology
- Nephrology
Background:
- Differentiated embryo-chondrocyte 2 (DEC2) is a transcriptional factor regulating gene expression.
- DEC2's role in kidney inflammatory responses is not fully understood.
Purpose of the Study:
- To investigate the role of DEC2 in human mesangial cells during inflammatory stimulation.
- To elucidate the regulatory pathway involving DEC2, double-stranded RNA, and inflammatory mediators.
Main Methods:
- Cultured human mesangial cells were treated with polyinosinic-polycytidylic acid (poly IC).
- RNA interference was used to knockdown DEC2 and Toll-like receptor 3 (TLR3).
- Expression levels of IFN-β, RIG-I, and CCL5 were measured.
Main Results:
- Poly IC treatment induced DEC2 expression in human mesangial cells.
- Knockdown of DEC2 enhanced poly IC-induced expression of IFN-β, RIG-I, and CCL5.
- Knockdown of TLR3 abolished poly IC-induced DEC2 expression.
Conclusions:
- DEC2 expression is induced by double-stranded RNA via TLR3 in human mesangial cells.
- DEC2 acts as a negative feedback regulator of the IFN-β/RIG-I/CCL5 inflammatory pathway in the glomerulus.
- DEC2 may play a role in controlling chronic kidney inflammation.
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