Metal ions are widely recognized as a key factor on conformational changes and aggregation of Alzheimers disease amyloid (Abeta). So far Al3+ received much less attention than other biometals in terms of interaction with beta-amyloid. Brain endothelial cells have been identified as important regulators of the neuronal microenvironment, including Abeta levels. The purpose of this study is to compare the effects of the complex amyloid (Abeta1-42)-Al, from human and rat, with the effects produced by metal-free Abeta on rat neuroendothelial cells (NECs). To establish Abeta and Abeta-Al toxicity NECs, survival, vitality, and angiogenesis are evaluated. Cells survival is reduced by human and rat Abeta in a time-dependent manner. This toxic effect is remarkably pronounced in the presence of human Abeta-Al. However, only rat Abeta has an anti-angiogenic properties on NECs, and this effect is dramatically aggravated using both human and rat Abeta-Al complexes. Based on the data and arguments herein presented, involvement of Al3+ in Abeta aggregation and consequently increasing endothelial cells toxicity is clearly demonstrated.
Comparative effects of Abeta(1-42)-Al complex from rat and human amyloid on rat endothelial cell cultures.
Ricchelli F;Tognon G;
2007
Abstract
Metal ions are widely recognized as a key factor on conformational changes and aggregation of Alzheimers disease amyloid (Abeta). So far Al3+ received much less attention than other biometals in terms of interaction with beta-amyloid. Brain endothelial cells have been identified as important regulators of the neuronal microenvironment, including Abeta levels. The purpose of this study is to compare the effects of the complex amyloid (Abeta1-42)-Al, from human and rat, with the effects produced by metal-free Abeta on rat neuroendothelial cells (NECs). To establish Abeta and Abeta-Al toxicity NECs, survival, vitality, and angiogenesis are evaluated. Cells survival is reduced by human and rat Abeta in a time-dependent manner. This toxic effect is remarkably pronounced in the presence of human Abeta-Al. However, only rat Abeta has an anti-angiogenic properties on NECs, and this effect is dramatically aggravated using both human and rat Abeta-Al complexes. Based on the data and arguments herein presented, involvement of Al3+ in Abeta aggregation and consequently increasing endothelial cells toxicity is clearly demonstrated.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.