Apoptosis of endothelial cells in vessels affected by cerebral vasospasm

Zubkov, Alexander Y.; Ogihara, Kotaro; Bernanke, David H.; Parent, Andrew D.; Zhang, Junyi

doi:10.1016/s0090-3019(99)00187-1

Cited by 78 publications

(49 citation statements)

References 25 publications

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“…In grade one patients following a SAH, the degree of injury is more subtle and is believed to be limited to apoptosis in more sensitive areas of the brain, for example the hippocampus. This has been demonstrated in both animal models and in patients post mortem (30,31,44,46,47).…”

Section: Yuksel S Et Al: Brain Injury Following Aneurysmal Subarachnmentioning

confidence: 82%

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Early brain injury following aneurysmal subarachnoid hemorrhage: emphasis on cellular apoptosis

Yuksel

Tosun²,

Cahill³

et al. 2012

Turkish Neurosurgery

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Subarachnoid hemorrhage (SAH) due to intracranial aneurysm rupture is a complex clinical disease with high mortality and morbidity. Recent studies suggest that early brain injury (EBI) rather than vasospasm might be responsible for morbidity and mortality within 24-72 hours after SAH. The rise in intracranial pressure following SAH causes a significant drop in cerebral perfusion pressure that leads to global cerebral ischemia and initiates the acute injury cascade. Various molecular mechanisms have been shown to involve in the pathophysiology of EBI including cellular apoptosis. In this review, we summarize apoptotic molecular mechanisms involved in the etiology of EBI and its potential as a target for future therapeutic intervention.KeywoRds: Apoptosis, Early brain injury, p53, Stroke, Subarachnoid hemorrhage ÖZIntrakraniyal anevrizma rüptürüne bağlı gelişen subaraknoid kanama (SAK), yüksek mortalite ve morbidite ile seyreden kompleks bir hastalıktır. Yakın zamanda yapılan çalışmalar SAK sonrası 24-72. saatler içinde gelişen morbidite ve mortaliteden vazospasmdan ziyade, erken beyin hasarının sorunlu olduğunu ileri sürmüştür. SAK sonrasında gelişen intrakraniyal basınç artışı, serebral perfüzyon basıncında ciddi düşüşe neden olup global serebral iskemi ile sonuçlanır ve akut hasar kaskadını başlatır. Hücresel apopitoz dahil pek çok moleküler mekanizmanın erken beyin hasarının (EBH) patofizyolojisinde rol oynadığı gösterilmiştir. Bu derlemede; EBH etiyolojisinde rol alan apopitotik mekanizmalar ve bunların gelecekte potansiyel tedavi hedefi olarak önemleri özetlenmiştir.

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Section: Yuksel S Et Al: Brain Injury Following Aneurysmal Subarachnmentioning

confidence: 82%

“…It has been shown that apoptosis occurs in the endothelial cells of vessels, the prevention of which can attenuate the degree of vasospasm (45). Apoptosis has been identified in a patient who died from a SAH (46).…”

Section: Apoptosis In Ebimentioning

confidence: 99%

Early brain injury following aneurysmal subarachnoid hemorrhage: emphasis on cellular apoptosis

Yuksel

Tosun²,

Cahill³

et al. 2012

Turkish Neurosurgery

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“…26 Endothelial apoptosis may also occur during cerebral vasospasm after SAH. 27 Furthermore, the extrinsic apoptotic signaling pathway that involves TNF-␣ and the downstream signaling molecule FADD seem to initiate vessel weakening and remodeling in human IAs. 16 Moreover, both TNF-␣-mediated extrinsic and Bcl-2-mediated intrinsic apoptotic pathways induced apoptosis in a rabbit aneurysm model.…”

Section: Discussionmentioning

confidence: 99%

Genomics of Human Intracranial Aneurysm Wall

Shi

Awad

Jafari

et al. 2009

Stroke

108

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Background and Purpose-The pathogenesis of intracranial aneurysms (IAs) remains elusive. Most studies have focused on individual genes, or a few interrelated genes or products, at a time in human IA. However, a broad view of pathologic mechanisms has not been investigated by identifying pathogenic genes and their interaction in networks. Our study aimed to analyze global gene expression patterns in the IA wall. Methods-To our knowledge, our group was the first to perform Illumina microarray analysis on human IA via comparison of aneurysm wall and superficial temporal artery tissues from 6 consecutive patients. We adopted stringent statistical criteria to the individual genes; genes with a false discovery rate Ͻ0.01 and Ͼ2-fold change were selected as differentially expressed. To identify the overrepresented biologic pathways with the differentially expressed genes, we performed hypergeometric testing of the genes selected by relaxed criteria of PϽ0.01 and fold change Ͼ1.5. Results-There are 326 distinct differentially expressed genes between IA and superficial temporal artery tissues (Ͼ2-fold change) with a false discovery rate Ͻ0.01. Analysis of the Kyoto Encyclopedia of Genes and Genomes pathways revealed the most impacted functional pathways: focal adhesion, extracellular matrix receptor interaction, and cell communication. Analysis of the Gene Ontology also supported the involvement of another 2 potentially important pathways: inflammatory response and apoptosis. Conclusions-The differentially expressed genes in the aneurysm wall may shed light on aneurysm pathobiology and provide novel targets for therapeutic intervention. These data will help generate hypotheses for future studies. (Stroke.

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“…21 We recently observed apoptotic changes in the endothelial cells in the middle cerebral artery of a patient who died of cerebral vasospasm after SAH. 22 Endothelial cells in the spastic arteries demonstrated condensation of the nucleus chromatin in transmission electron microscopy and stained positive to terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay.…”

Section: Discussionmentioning

confidence: 99%

Caspase Inhibitors Attenuate Oxyhemoglobin-Induced Apoptosis in Endothelial Cells

Meguro

Chen

Parent

et al. 2001

Stroke

Self Cite

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Background and Purpose-Our recent study showed that oxyhemoglobin (OxyHb) induces apoptosis in cultured endothelial cells. Apoptosis requires the action of various classes of proteases, including a family of cysteine proteases known collectively as the caspases. This study was undertaken to investigate the effect of 2 caspase inhibitors, Z-VDVAD-FMK and Z-DEVD-FMK, in the protection of endothelial cells from OxyHb-induced apoptosis. Methods-Cultured bovine brain microvascular endothelial cells (passages 5 to 9) were exposed to OxyHb (10 mol/L) for 24 to 72 hours with and without caspase inhibitors. Cell attachment, DNA ladder, Western blotting of poly(ADP-ribose) polymerase (PARP), and caspase activities were measured to confirm the cytotoxic effect of OxyHb and the protective effect of the caspase inhibitors.

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Apoptosis of endothelial cells in vessels affected by cerebral vasospasm

Cited by 78 publications

References 25 publications

Early brain injury following aneurysmal subarachnoid hemorrhage: emphasis on cellular apoptosis

Early brain injury following aneurysmal subarachnoid hemorrhage: emphasis on cellular apoptosis

Genomics of Human Intracranial Aneurysm Wall

Caspase Inhibitors Attenuate Oxyhemoglobin-Induced Apoptosis in Endothelial Cells

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