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Effect of CDK8 to TGF-β/BMP Signaling Pathway in Nervous System
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  • Yuheng Zhang,
  • Hua Mei,
  • Yanbo Zhang,
  • Meiqi Wang,
  • Yanan Hu,
  • Hong Cui
Yuheng Zhang
The Affiliated Hospital of Inner Mongolia Medical University

Corresponding Author:[email protected]

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Hua Mei
The Affiliated Hospital of Inner Mongolia Medical University
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Yanbo Zhang
The Affiliated Hospital of Inner Mongolia Medical University
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Meiqi Wang
The Affiliated Hospital of Inner Mongolia Medical University
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Yanan Hu
The Affiliated Hospital of Inner Mongolia Medical University
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Hong Cui
Capital Medical University Affiliated Beijing Friendship Hospital
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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.