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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Endothelial effects of 3-hydroxyglutaric acid: implications for glutaric aciduria type I.

Infants with glutaric aciduria type 1 (GA1) are subject to intracranial vascular dysfunction. Here, we demonstrate that the disease-specific metabolite 3-hydroxyglutaric acid (3-OH-GA) inhibits basal and vascular endothelial growth factor (VEGF)-induced endothelial cell migration. 3-OH-GA affects the morphology of VEGF-induced endothelial tubes in vitro because of partial disintegration of endothelial cells. These effects correlate with Ve-cadherin loss. Remarkably, 3-OH-GA treatment of human dermal microvascular endothelial cells leads to disruption of actin cytoskeleton. Local application of 3-OH-GA alone or in combination with VEGF in chick chorioallantoic membrane induces abnormal vascular dilatation and hemorrhage in vivo. The study demonstrates that 3-OH-GA reduces endothelial chemotaxis and disturbs structural vascular integrity in vitro and in vivo. These data may provide insight in the mechanisms of 3-OH-GA-induced vasculopathic processes and suggest N-methyl-D-aspartate receptor-dependent and -independent pathways in the pathogenesis of GA1.[1]

References

  1. Endothelial effects of 3-hydroxyglutaric acid: implications for glutaric aciduria type I. Mühlhausen, C., Ott, N., Chalajour, F., Tilki, D., Freudenberg, F., Shahhossini, M., Thiem, J., Ullrich, K., Braulke, T., Ergün, S. Pediatr. Res. (2006) [Pubmed]
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