Abstract
Several studies have demonstrated a potential interaction between mesenchymal stem cells (MSCs) and saccular aneurysms. In this study, we sought to determine whether allogenic bone marrow-derived MSCs had the ability to prevent aneurysm formation in a known rabbit elastase aneurysm model. MSCs were injected intravenously in experimental rabbits at the time of surgical creation and two weeks postcreation and compared with control rabbits receiving vehicle injection. Angiography was used to compare aneurysm measurements four weeks postcreation, and aneurysms were harvested for histological properties. Serum was collected longitudinally to evaluate cytokine alterations. Serum from control animals was also utilized to perform in vitro tests with MSCs to compare the effect of the serologic environment in animals with and without aneurysms on MSC proliferation and cytokine production. While aneurysm morphometric comparisons revealed no differences, significant cytokine alterations were observed in vitro and in vivo, suggesting both anti-inflammatory and proinflammatory processes were occurring in the presence of MSCs. Histological analyses suggested that tunica intima hyperplasia was inhibited in the presence of MSCs.
Highlights
It is estimated that approximately 3% of the general population harbors and intracranial saccular aneurysm, a pathological dilation of the cerebral arteries at bifurcation points that is prone to rupturing [1]
Several key changes in the arterial wall occur that are thought to lead to aneurysm formation, including loss of elastin content in the internal elastic lamina and reduction of the tunica media leading to weakening of the wall [3]
The pathogenesis of aneurysms is a complex process involving many inflammatory cascades which may have been impacted by the IV injection of mesenchymal stem cells (MSCs)
Summary
It is estimated that approximately 3% of the general population harbors and intracranial saccular aneurysm, a pathological dilation of the cerebral arteries at bifurcation points that is prone to rupturing [1]. Aneurysmal rupture occurs in 10 of every 100,000 people annually and carries with it an estimated mortality rate of 50% and a significant neurological disability rate among survivors of approximately 30% [2]. Many prevention strategies have aimed at disrupting the implicated inflammatory cascades. They have been fraught with limited success or impossible human application and have largely been focused on abdominal aortic fusiform aneurysms [6,7,8,9,10,11,12,13,14]. There is evidence to suggest that saccular and fusiform aneurysms
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