Role of VE-Cadherin and p120-catenin in the formation of experimental intracranial aneurysms in animals.

BACKGROUND: Dysfunction of endothelial cells (ECs) constitutes a critical factor in formatting intracranial aneurysms (IAs). However, little is known about the response of ECs to hemodynamic insults and its contribution to IA formation.

METHODS AND MATERIAL: IAs models were constructed in both adult female New Zealand white rabbits and male Sprague-Dawley rats. Morphological changes of vessel wall were detected by HE staining. Molecular and cellular changes, including P120ctn and VE-Cadherin, in the median sagittal section of the artery bifurcation were analyzed by fluorescent staining.

RESULTS: Destructive aneurysmal remodeling and the formation of morphological IAs can be observed at the basilar termini of experimental rabbits, and anterior cerebral artery-olfactory artery bifurcation of rats. The expression of P120ctn co-localized with VE-Cadherin in ECs decreased. Moreover, the expression of P120ctn co-localized with nucleus of ECs increased. These events suggested that P120ctn were transformed membrane to nucleus of ECs.

CONCLUSION: The potential mechanism, that IAs are always localizing in the bifurcation apices, maybe that the endothelium injury of vessel wall can be induced by different hemodynamic conditions. Hemodynamic changes in artery bifurcation may initiate the formation of IAs.