Effect of CDK8 to TGF-β/BMP Signaling Pathway in Nervous System

Abstract

Aim: To research the relationship among CDK8, TGF-β/BMP signaling pathway and apoptosis in nervous system. Methods: Mouse neuronal cells (NE4C) were subcultured. CDK8 was overexpressed and silenced (overexpressed plasmid was pcDNA3.1(+), silenced plasmid was pGPU6-si103). The factors (TGF-β1, Smad2, Smad3, BMP6, BMP7, Smad1, Smad5, Smad8) of TGF-β/BMP signaling pathway were detected by qRT-PCR. Western blotting was used to test the caspase1 and caspase3. Resluts: The overexpression of CDK8 can cause that TGF-β1, Smad2, Smad3, BMP6, BMP7, Smad1, Smad5 and Smad8 were increased obviously. After CDK8 silencing, TGF-β1, Smad2, Smad3, BMP6, BMP7, Smad1 and Smad8 decreased, except Smad5. The overexpression of CDK8 can lead to a rise of caspase1, but caspase3 was only an upward trend. After CDK8 expressed silencing, caspase1 increased significantly, and caspase3 tended to increasing. Conclusion: In the nervous system, CDK8 positively regulates TGF-β/BMP signaling pathway, and apoptosis is one of their downstream mechanisms.