Prolonged shear stress and KLF2 suppress constitutive proinflammatory transcription through inhibition of ATF2.

@article{Fledderus2007ProlongedSS,
  title={Prolonged shear stress and KLF2 suppress constitutive proinflammatory transcription through inhibition of ATF2.},
  author={Joost O. Fledderus and Johannes V. van Thienen and Reinier A Boon and Rob J. Dekker and Jakub Rohlena and Oscar L. Volger and Ann-Pascale J J Bijnens and Mat J. A. P. Daemen and J. J. W. Kuiper and Theo J. C. van Berkel and H. Pannekoek and Anton J. G. Horrevoets},
  journal={Blood},
  year={2007},
  volume={109 10},
  pages={4249-57}
}
Absence of shear stress due to disturbed blood flow at arterial bifurcations and curvatures leads to endothelial dysfunction and proinflammatory gene expression, ultimately resulting in atherogenesis. KLF2 has recently been implicated as a transcription factor involved in mediating the anti-inflammatory effects of flow. We investigated the effect of shear on basal and TNF-alpha-induced genomewide expression profiles of human umbilical vein endothelial cells (HUVECs). Cluster analysis confirmed… CONTINUE READING

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