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Arteriovenous malformations of the brain may arise due to a genetic mutation, acquired later in life, that activates a cellular signaling pathway in endothelial cells -- the same one that drives tumor formation, a study showed.
Researchers led by Sergey Nikolaev, PhD, of University of Geneva Medical School, reported in the New England Journal of Medicine that expression of mutant KRAS (KRASG12V) in endothelial cells in vitro induced increased extracellular signal-regulated kinase (ERK) activity, increased expression of genes related to angiogenesis and Notch signaling, and enhanced migratory behavior.
"We propose that these malformations develop as a result of KRAS-induced activation of the MAPK-ERK signaling pathway in brain endothelial cells," Nikolaev's group wrote, suggesting that active KRAS "dysregulates angiogenesis and vascular remodeling in endothelial cells."
"How might alterations in RAS signaling in endothelial cells induce arteriovenous malformations?
Even if not all arteriovenous malformation samples showed activating KRAS mutations, they still had more MAPK-ERK signaling in endothelial cells.
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