intracranial aneurysm/protease

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Absence of plasma protease-antiprotease imbalance in the formation of saccular cerebral aneurysms.

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OBJECTIVE We examined the hypothesis that a plasma protease-antiprotease imbalance contributes to the formation of saccular cerebral aneurysms and the suggestion that the assay of these enzymes might be a screening tool for people at higher risk for aneurysm formation. METHODS From June 1997 through

Increased apoptosis and cysteinyl aspartate specific protease-3 gene expression in human intracranial aneurysm.

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OBJECTIVE To investigate apoptosis in vascular smooth muscle cells (VSMCs) and caspase-3 expression in ruptured intracranial aneurysm. METHODS Tissue samples of 15 ruptured intracranial aneurysms, 6 abdominal aortic aneurysms (AAA) and 6 normal vessels were evaluated. Apoptosis in VSMCs was

Alpha 1-antitrypsin deficiency in intracranial aneurysms and cervical artery dissection.

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The pathogenesis of ruptured intracranial aneurysms and cervical artery dissections is poorly understood but may be similar in these two disorders. We report four patients with alpha 1-antitrypsin deficiency who developed a ruptured intracranial aneurysm or spontaneous dissection of the cervical

The alanine/threonine polymorphism of the alpha-1-antichymotrypsin (SERPINA3) gene and ruptured intracranial aneurysms in the Japanese population.

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BACKGROUND Serine protease inhibitor member 3 of clade A (SERPINA3), also known as alpha-1-antichymotrypsin, inhibits the activity of cathepsin G. The release of neutrophil cathepsin G (proteolytic enzyme) can destroy the vascular matrix through degradation, platelet aggregation and coagulation

Polymorphism rs4934 of SERPINA3 and sporadic intracranial aneurysms in the Chinese population.

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BACKGROUND Serine protease inhibitor member 3 of clade A (SERPINA3) has been shown as a risk factor for aneurysmal subarachnoid hemorrhage in a Polish population. In the present study, the authors investigated the correlation between the rs4934 polymorphism of SERPINA3 and sporadic intracranial

Collagen cross-linkage, elastolytic and collagenolytic activities in cerebral aneurysms: a preliminary investigation.

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The pathogenesis of aneurysms formation and rupture is not clearly understood and is undoubtedly a multifactorial event. It is generally accepted that the aneurysm arises from an interaction between structural weakness of arterial wall and hemodynamic factors. Previous studies suggested the possible

Serum elastase and alpha-1-antitrypsin levels in patients with ruptured and unruptured cerebral aneurysms.

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Despite advances in surgical treatment and postoperative care, subarachnoid hemorrhage from ruptured cerebral aneurysms remains a devastating event. Excellent surgical results in treating unruptured aneurysms suggest the utility of screening tests to identify high-risk individuals. Unfortunately,

Intracranial Aneurysm Biomarker Candidates Identified by a Proteome-Wide Study

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The scientific basis of intracranial aneurysm (IA) formation, its rupture and further development of cerebral vasospasm is incompletely understood. Aberrant protein expression may drive structural alterations of vasculature found in IA. Deciphering the molecular mechanisms underlying these events

Elastin degradation in the superficial temporal arteries of patients with intracranial aneurysms reflects changes in plasma elastase.

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OBJECTIVE alpha 1-Antitrypsin (AAT) and alpha 2-macroglobulin (AMG) are elastase inhibitors that bind the enzyme and reduce measured levels of free elastase. It was recently demonstrated that some patients with intracranial aneurysms have significantly elevated plasma elastase (PE) levels. Although

Vascular extracellular matrix remodeling in cerebral aneurysms.

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OBJECTIVE The occurrence of cerebral aneurysms has been linked to alterations in the extracellular matrix and to matrix-degrading proteases. The purpose of the present study was to determine whether active extracellular matrix remodeling occurs within cerebral aneurysms. METHODS Aneurysm tissue was

Flow-induced, inflammation-mediated arterial wall remodeling in the formation and progression of intracranial aneurysms.

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Unruptured intracranial aneurysms (UIAs) are relatively common lesions that may cause devastating intracranial hemorrhage, thus producing considerable suffering and anxiety in those affected by the disease or an increased likelihood of developing it. Advances in the knowledge of the

Alpha 1-antitrypsin activity in subarachnoid hemorrhage.

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An altered equilibrium of protease/protease-inhibitor factors may be involved in the pathogenesis of aneurysm rupture: alpha 1-antitrypsin (alpha 1-AT) represents the most relevant inhibitor of elastase, a proteolytic enzyme enhancing catabolic processes of collagen metabolism. In the present study

Matrix metalloproteinases in cerebrovascular diseases.

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Matrix metalloproteinases are important factors for tissue remodelling and are activated during several physiological and pathological conditions, including cerebrovascular diseases. We give an overview of the structure, production and physiological effects of these widely distributed proteases and

Inactivation of alpha1-antiproteinase (alpha1-AT) and changes in antioxidants' plasma levels in subarachnoid hemorrhage.

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Recent studies have suggested that a quantitative or a qualitative imbalance between the activity of proteases and its inhibitors hypothetically might be involved in intracranial aneurysm rupture. In the present study we test the hypothesis that the systemic reduction of alpha1-antitrypsin activity

[Epidemiology and pathophysiology of spontaneous cervical artery dissection].

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Spontaneous cervical artery dissections are produced by the penetration of circulating blood into the vessel wall of one or more cervical arteries, without a preceding major trauma. Dissection is one of the most frequent etiologies of ischemic stroke in young patients. Its annual incidence is about

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