Expression of Structural Proteins and Angiogenic Factors in Cerebrovascular Anomalies

“…VaskŸler malformasyonlar dinamik lezyonlar olarak bilinmelerine raÛmen, bu lezyonlardaki angiogenezle ilgili az sayÝda •alÝßma mevcuttur (2). Angiogenezi dŸzen-leyen faktšrler bŸyŸme faktšrleri ve ekstrasellŸler matriks proteinleridir.…”

Section: Tartiþmaunclassified

“…Bu nedenle immatŸr damarlar fibronektinden zengin matriks i•erirken, matŸr damarlar lamininden zengin matriks i•erirler. KÝlÝ• ve arkadaßlarÝ •alÝßmalarÝnda AVMÕlerde KAÕlara oranla daha yŸksek laminin ekspresyonu saptamÝßlardÝr (2).…”

Section: Tartiþmaunclassified

“…Sonnstein ve arkadaßlarÝ pediatrik grupta yer alan ve nŸkseden 4 AVM olgusunda VEGF ekspresyonu saptamÝßlardÝr. KÝlÝ• ve arkadaßlarÝ ise, damarlar arasÝndaki gliotik beyin dokusunda saptanan bŸyŸme faktšr ekspresyonunun angiogenezin devamÝndan sorumlu olabileceÛini vurgulamÝßlardÝr (2).…”

Section: Tartiþmaunclassified

“…FarklÝ •alÝßmalarda, hipoksinin angiogenezi uyaran bir faktšr olduÛu vurgulanmÝßtÝr. Bu bulguyu destekler bi•imde AVM'lerde damarlar arasÝndaki beyin dokusunun da iskemik šzellikte olduÛu bilinmektedir (2). Son •alÝßmalar, kanamanÝn eßlik ettiÛi beyin tŸmšrle-rinde angiogenetik bŸyŸme faktšrlerinin varlÝÛÝnÝ gšs-termektedir.…”

Section: Tartiþmaunclassified

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Beyinde Vasküler Malformasyona Bağlı Kanama Nedeni ile Ani Ölen Üç Olgu Sunumu

et al. 2003

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…ZET SUMMARYVessel abnormalities seen in the central nervous system are the result of vascular malformations in brain and can be observed in various forms like little lesions determined at the autopsy to lesions leading to fatal intracranial haemorrhages. Our study includes three sudden death cases which were autopsied between 1998-2003 at the Morgue Specialization Department of the Council of Forensic Medicine. Cause of death was subarachnoidal and intracerebral haemorrhage due to vascular malformation in brain for all three cases. Age of our cases were between 16 to 29, two of them were male, and one was female. Macroscopic examination revealed softening of brain and cerebellum consistency, and inner parenchymal, intraventricular and subarachnoid hemorrhage areas with localisation on right parietal lobe in one case, and with localisation on cerebellum and brain stem in two cases. Microscopic examination showed folded vessel structures, connected and back to back with each other in brain parenchyma. Some of the vessels were thin walled and venous, but most of them were composed of ambigious vessel structures. Neural tissue could be differentiated between vessels. According to macroscopic and microscopic findings, the cases were considered as arteriovenous malformation, and related were subarachnoid and intracerebral hemorrhage. De-

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Evidence for endothelial‐to‐mesenchymal transition in human brain arteriovenous malformations

Shoemaker

McCormick

Allen

et al. 2020

Clinical & Translational Med

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Background Brain arteriovenous malformations (AVMs) are rare, potentially devastating cerebrovascular lesions that can occur in both children and adults. AVMs are largely sporadic and the basic disease biology remains unclear, limiting advances in both detection and treatment. This study aimed to investigate human brain AVMs for endothelial‐to‐mesenchymal transition (EndMT), a process recently implicated in cerebral cavernous malformations (CCMs). Methods We used 29 paraffin‐embedded and 13 fresh/frozen human brain AVM samples to profile expression of panels of EndMT‐associated proteins and RNAs. CCMs, a cerebrovascular disease also characterized by abnormal vasculature, were used as a primary comparison, given that EndMT specifically contributes to CCM disease biology. AVM‐derived cell lines were isolated from three fresh, surgical AVM samples and characterized by protein expression. Results We observed high collagen deposition, high PAI‐1 expression, and expression of EndMT‐associated transcription factors such as KLF4, SNAI1, and SNAI2 and mesenchymal‐associated markers such as VIM, ACTA2, and S100A4. SMAD‐dependent TGF‐β signaling was not strongly activated in AVMs and this pathway may be only partially involved in mediating EndMT. Using serum‐free culture conditions, we isolated myofibroblast‐like cell populations from AVMs that expressed a unique range of proteins associated with mature cell types and with EndMT. Conditioned medium from these cells led to increased proliferation of HUVECs and SMCs. Conclusions Collectively, our results suggest a role for EndMT in AVM disease. This may lead to new avenues for disease models to further our understanding of disease mechanisms, and to the development of improved diagnostics and therapeutics.

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Expression of Structural Proteins and Angiogenic Factors in Cerebrovascular Anomalies

Cited by 170 publications

References 54 publications

Central Nervous System Vascular Malformations

Central Nervous System Vascular Malformations

Beyinde Vasküler Malformasyona Bağlı Kanama Nedeni ile Ani Ölen Üç Olgu Sunumu

Evidence for endothelial‐to‐mesenchymal transition in human brain arteriovenous malformations

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