Inflammation has emerged as a vital component of the pathophysiology of intracranial aneurysms. Mast cells have been identified previously in human intracranial aneurysm tissues, and their presence was correlated with wall degeneration and intramural microhemorrhage. This study aimed to investigate whether mast cells can be used as a therapeutic target for the prevention of aneurysm rupture.
Adult mice were induced to intracranial aneurysms, using an amalgamation of a single injection of elastase into the cerebrospinal fluid and induced systemic hypertension. Aneurysm formation and rupture were assessed over three weeks. Roles of mast cells were assessed using a mast cell activator (C48/80), cromolyn, and KitW-sh/W-sh mice. The mast cell activation with C48/80 increased the rupture rate of aneurysms significantly (25% vs. 100%), without having an effect on the overall aneurysm formation rate. Furthermore, mast cells’ genetic deficiency significantly prevented aneurysm rupture (25% vs. 80%, KitW-sh/W-sh vs. wild-type mice).
In conclusion, this study demonstrated the function of mast cells in the advancement of intracranial aneurysm rupture, and might serve as a potential therapeutic target for its prevention. Further clinical and mechanistic studies are requisite to further establish the contribution of mast cells to the development of subarachnoid hemorrhage and aneurysmal rupture.
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