Journal of Neural Transmission

, Volume 114, Issue 7, pp 867–875

Human TIEG2/KLF11 induces oligodendroglial cell death by downregulation of Bcl-XL expression

Authors

  • Z. Wang
    • Center of Anatomy, Department of NeuroanatomyUniversity of Goettingen
  • B. Spittau
    • Center of Anatomy, Department of NeuroanatomyUniversity of Goettingen
  • M. Behrendt
    • Center of Anatomy, Department of NeuroanatomyUniversity of Goettingen
  • B. Peters
    • Department of AnatomyUniversity of Saarland
  • K. Krieglstein
    • Center of Anatomy, Department of NeuroanatomyUniversity of Goettingen
Article

DOI: 10.1007/s00702-007-0635-6

Cite this article as:
Wang, Z., Spittau, B., Behrendt, M. et al. J Neural Transm (2007) 114: 867. doi:10.1007/s00702-007-0635-6

Summary

TGF-β-induced apoptosis is essential for embryonic development and mainteanance of adult tissues. Impairment of the apoptotic pathway, regulated by TGF-β, plays a center role in tumorigenesis and manifestations of different diseases. TIEG2/KLF11 is a recently identified human TGF-β-inducible zinc finger protein belonging to the family of Sp1/KLF-like transcription factors. In human and murine tissues it has been shown that TIEG1 and TIEG2 induce apoptosis and inhibit cell growth. Since TGF-β and Tieg1 are able to induce apoptosis in the oligodendroglial cell line OLI-neu, we analysed the ability of TIEG2 to mimic the effects observed after treatment with TGF-β and overexpression of Tieg1. Herein we report that TIEG2 induces Caspase3-dependent apoptosis in murine OLI-neu cells. Furthermore, we could demonstrate that TIEG2 decreases the levels of the anti-apoptotic protein Bcl-XL and inhibits transcription driven by the Bcl-XL promoter. These data suggest that TIEG2 serves as a downstream mediator of TGF-β, bridging TGF-β-dependent signaling to the intracellular pathway of apoptosis.

Keywords: TIEG2/KLF11, TGF-β, apoptosis, Bcl-XL, Bcl-2, Caspase3, zinc finger, OLI-neu

Copyright information

© Springer-Verlag 2007