Proliferative Activity through Extracellular Signal-regulated Kinase of Smooth Muscle Cells in Vascular Walls of Cerebral Arteriovenous Malformations

Takagi, Yasushi; Kikuta, Ken-ichiro; Sadamasa, Nobutake; Nozaki, Kazuhiko; Hashimoto, Nobuo

doi:10.1227/01.neu.0000192167.54627.3a

Cited by 31 publications

(16 citation statements)

References 26 publications

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“…Caspasedependent apoptosis and overproduction of matrix metalloproteinase have been implicated as contributory mechanisms in the associated degradation or remodeling of the arterial wall. 12,13 Therefore, diffuse and severe thinning of the wall area in our patients with MMD with could represent media shrinkage, which was not observed in our patients with ICAD.…”

Section: Discussionmentioning

confidence: 63%

High-Resolution Magnetic Resonance Wall Imaging Findings of Moyamoya Disease

Ryoo

Cha

Kim

et al. 2014

Stroke

161

103

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Background and Purpose-Diagnosis of Moyamoya disease (MMD) is based on the characteristic angiographic findings.However, differentiating MMD from intracranial atherosclerotic disease (ICAD) is difficult. We compared vessel wall imaging findings on high-resolution magnetic resonance imaging between MMD and ICAD. Methods-High-resolution magnetic resonance imaging was performed on 32 patients with angiographically proven MMD and 16 patients with acute infarcts because of ICAD. Bilateral internal carotid arteries and steno-occlusive middle cerebral artery were analyzed for wall enhancement and remodeling. Results-Enhancement patterns and distribution were different. Most patients with MMD (90.6%) showed concentric enhancement on distal internal carotid arteries and middle cerebral arteries, whereas focal eccentric enhancement was observed on the symptomatic segment in ICAD. MMD was characterized by middle cerebral artery shrinkage; the remodeling index and wall area were lower in MMD than in ICAD (remodeling index, 0.19±0.11 versus 1.00±0.43; wall area, 0.32±0.22 versus 6.00±2.72; P<0.001). Conclusions-MMD

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Section: Discussionmentioning

confidence: 63%

High-Resolution Magnetic Resonance Wall Imaging Findings of Moyamoya Disease

Ryoo

Cha

Kim

et al. 2014

Stroke

161

103

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“…17 In and around the vessel walls of AVMs, various growth factors, including vascular endothelial growth factor, basic fibroblast growth factor, and transforming growth factor-b 1 , are observed. [18][19][20] Proliferation-related transcription factors, such as hypoxia-inducing factor and extracellular signal-regulated protein kinase, are expressed, 21,22 and endothelial proliferation takes place in vascular walls. 21 Cell death (via apoptotic pathways) is also detected in the vessel walls of cerebral AVMs.…”

Section: Discussionmentioning

confidence: 99%

Activation of Nuclear Factor κB in Cerebral Arteriovenous Malformations

et al. 2010

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“…1,8,25,89 After stimulation, ERK induces cellular proliferation and transformation. 25,89,110,134 Takagi and colleagues 124 have suggested that the activation of the ERK pathway depends on the chronic increase in blood flow within the vasculature. It has been well established that chronic increases in blood flow can upregulate shear-induced genes, which induce vascular remodeling.…”

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confidence: 99%

Cerebral arteriovenous malformations. Part 1: cellular and molecular biology

Moftakhar

Hauptman

Malkasian

et al. 2009

FOC

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Object The scientific understanding of the nature of arteriovenous malformations (AVMs) in the brain is evolving. It is clear from current work that AVMs can undergo a variety of phenomena, including growth, remodeling, and/or regression—and the responsible processes are both molecular and physiological. A review of these complex processes is critical to directing future therapeutic approaches. The authors performed a comprehensive review of the literature to evaluate current information regarding the genetics, pathophysiology, and behavior of AVMs. Methods A comprehensive literature review was conducted using PubMed to reveal the molecular biology of AVMs as it relates to their complex growth and behavior patterns. Results Growth factors involved in AVMs include vascular endothelial growth factor, fibroblast growth factor, transforming growth factor β, angiopoietins, fibronectin, laminin, integrin, and matrix metalloproteinases. Conclusions Understanding the complicated molecular milieu of developing AVMs is essential for defining their natural history. Growth factors, extracellular matrix proteins, and other molecular markers will be the key to unlocking novel targeted drug treatments for these brain malformations.

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Proliferative Activity through Extracellular Signal-regulated Kinase of Smooth Muscle Cells in Vascular Walls of Cerebral Arteriovenous Malformations

Abstract: pERK was detected in smooth muscle cells of the vascular walls of AVMs. It may function in the proliferative activity of smooth muscle cells. Vascular remodeling through pERK may play an important role in the growth and maintenance of cerebral vascular malformations.

Cited by 31 publications

References 26 publications

High-Resolution Magnetic Resonance Wall Imaging Findings of Moyamoya Disease

High-Resolution Magnetic Resonance Wall Imaging Findings of Moyamoya Disease

Activation of Nuclear Factor κB in Cerebral Arteriovenous Malformations

Cerebral arteriovenous malformations. Part 1: cellular and molecular biology

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