Hemodynamic Force as a Potential Regulator of Inflammation-Mediated Focal Growth of Saccular Aneurysms in a Rat Model.

Past studies have elucidated the crucial role of macrophage-mediated inflammation in the growth of intracranial aneurysms (IAs), but the contributions of hemodynamics are unclear. Considering the size of the arteries, we induced de novo aneurysms at the bifurcations created by end-to-side anastomoses with the bilateral common carotid arteries in rats. Sequential morphological data of induced aneurysms were acquired by magnetic resonance angiography.

Involvement of neutrophils in machineries underlying the rupture of intracranial aneurysms in rats.

Subarachnoid hemorrhage due to rupture of an intracranial aneurysm has a quite poor prognosis after the onset of symptoms, despite the modern technical advances. Thus, the mechanisms underlying the rupture of lesions should be clarified. To this end, we obtained gene expression profile data and identified the neutrophil-related enriched terms in rupture-prone lesions using Gene Ontology analysis.

The Bilateral Ovariectomy in a Female Animal Exacerbates the Pathogenesis of an Intracranial Aneurysm.

Considering the poor outcome of subarachnoid hemorrhage (SAH) due to the rupture of intracranial aneurysms (IA), mechanisms underlying the pathogenesis of IAs, especially the rupture of lesions, should be clarified. In the present study, a rat model of IAs in which induced lesions spontaneously ruptured resulting in SAH was used. In this model, the combination of the female sex and the bilateral ovariectomy increased the incidence of SAH, similar to epidemiological evidence in human cases.

Dedifferentiation of smooth muscle cells in intracranial aneurysms and its potential contribution to the pathogenesis.

Smooth muscle cells (SMCs) are the major type of cells constituting arterial walls and play a role to maintain stiffness via producing extracellular matrix. Here, the loss and degenerative changes of SMCs become the major histopathological features of an intracranial aneurysm (IA), a major cause of subarachnoid hemorrhage. Considering the important role of SMCs and the loss of this type of cells in IA lesions, we in the present study subjected rats to IA models and examined how SMCs behave during disease progression.

Eicosapentaenoic acid prevents the progression of intracranial aneurysms in rats.

Background: As subarachnoid hemorrhage due to rupture of an intracranial aneurysm (IA) has quite a poor outcome despite of an intensive medical care, development of a novel treatment targeting unruptured IAs based on the correct understanding of pathogenesis is mandatory for social health.

Methods: Using previously obtained gene expression profile data from surgically resected unruptured human IA lesions, we selected G-protein coupled receptor 120 (GPR120) as a gene whose expression is significantly higher in lesions than that in control arterial walls. To corroborate a contribution of GPR120 signaling to the pathophysiology, we used an animal model of IAs and examine the effect of a GPR120 agonist on the progression of the disease.

High-Fat Diet Intake Promotes the Enlargement and Degenerative Changes in the Media of Intracranial Aneurysms in Rats.

Subarachnoid hemorrhage due to rupture of intracranial aneurysms is a life-threatening disease. Although some previous reports have demonstrated an association between lipid accumulation and degenerative changes in aneurysmal walls in humans, epidemiological studies have failed to identify dyslipidemia as a risk factor for intracranial aneurysms. Thus, we examined whether an increase in serum cholesterol levels facilitates the progression of intracranial aneurysms in a rat model.

Macrophage Imaging of Intracranial Aneurysms.

Considered with a poor outcome of subarachnoid hemorrhage due to rupture of intracranial aneurysms (IAs), treatment interventions to prevent rupture of the lesions are mandatory for social health. As treatment option is limited to surgical manipulations, like microsurgical clipping, endovascular coiling or deployment of flow diverter, and these surgical interventions have a potential risk of complications in nature, a proper selection of rupture-prone IAs among ones incidentally found is essential. Today, a rupture risk in each case is estimated by several factors like patient characteristics and morphological ones of each lesion.

KRAS G12D or G12V Mutation in Human Brain Arteriovenous Malformations.

Background: Brain arteriovenous malformations (BAVMs) are vascular malformations composed of tangles of abnormally developed vasculature without capillaries. Abnormal shunting of arteries and veins is formed, resulting in high-pressure vascular channels, which potentially lead to rupture. BAVMs are generally considered a congenital disorder.

Intracranial Aneurysm as a Macrophage-mediated Inflammatory Disease.

Subarachnoid hemorrhage (SAH) is mainly attributable to the rupture of intracranial aneurysms (IAs). Although the outcome of SAH is considerably poor in spite of the recent intensive medical care, mechanisms regulating the progression of IAs or triggering rupture remain to be clarified, making the development of effective preemptive medicine to prevent SAH difficult. However, a series of recent studies have been expanding our understanding of the pathogenesis of IAs.