Preventing Atherosclerosis Is All About Going With The Flow
In a study appearing online on December 8 in advance of print publication in the January 2006 issue of the Journal of Clinical Investigation, Guillermo Garcia-Carde?a and colleagues from Harvard Medical School show that this resistance is based in part on the induction of the transcription factor KLF2 by distinct blood flow patterns in these regions.
Previous studies have shown that blood flow-induced shear stress on the vessel wall is transduced into a biochemical signal that can cause changes in the vessel wall that may protect against or make a vessel prone to atherosclerosis.
Garcia-Carde?a et al. show that the transcription factor KLF2 (Kruppel-like factor 2) is selectively induced in endothelial cells lining the vessel wall by arterial blood flow patterns that mimic the hemodynamic environment in the atheroprotected regions of the human carotid artery.
This flow-mediated increase in KLF2 expression occurs via a MEK5/ERK5/MEF2 signaling pathway. Increased KLF2 activity helps regulate inflammation, clot formation, and new vessel growth.
These data suggest that KLF2 acts as a mechanically-activated transcription factor that is important for integrating multiple functions of cells of the vessel wall in regions of the blood vessel network that are relatively resistant to the development of atherosclerosis.
TITLE: Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2
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Journal of Clinical Investigation - Dec 8th
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