Acute alterations in microvascular basal lamina after subarachnoid hemorrhage

Sehba, Fatima A.; Mostafa, Gulam; Knopman, Jared; Friedrich, Victor L.; Bederson, Joshua B.

doi:10.3171/jns.2004.101.4.0633

Cited by 117 publications

(89 citation statements)

References 63 publications

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“…SAH causes profound reductions in cerebral blood flow (CBF), reduced cerebral autoregulation, and acute cerebral ischemia. [122][123][124][125][126] These pathophysiological processes are linked to raised intracranial pressure and decreased cerebral perfusion pressure, 122,127,128 decreased availability of nitric oxide, 126,129 acute vasoconstriction 123,130,131 and microvascular platelet aggregation, 132 activation of microvascular collagenases, loss of microvascular collagen, 133 and endothelial barrier antigen leading to decreased microvascular perfusion and increased permeability. 132,133 Despite recent advances in the understanding of the mechanisms of SAH-induced brain injury, few effective treatments exist, and further research is needed.…”

Section: Prevention Of Sahmentioning

confidence: 99%

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Bederson¹,

Connolly²,

Batjer³

et al. 2009

Stroke

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1,163

488

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Section: Prevention Of Sahmentioning

confidence: 99%

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Bederson¹,

Connolly²,

Batjer³

et al. 2009

Stroke

Self Cite

1,163

488

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“…Inoue [39] and Inoue and Kisilevski [40] reported abundant microfibril-like β-amyloid in the basement membrane in the cerebrovascular amyloid angiopathy of Alzheimer's disease. Sehba et al [75] demonstrated an acute loss of collagen IV from the cerebral microvasculature after aneurysmal subarachnoid haemorrhage.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural alterations of human cortical capillary basement membrane in human brain oedema

Castejón¹

2014

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“…7,11,22,23,28 MMP-9 levels in CSF and peripheral blood were significantly increased in patients with SAH. 11,22 MMP-9 degrades the extracellular matrix proteins of cerebral microvessel basal lamina and interendothelial tight junction proteins such as ZO-1, causing BBB disruption and brain edema formation.…”

Section: Discussionmentioning

confidence: 97%

“…11,22 MMP-9 degrades the extracellular matrix proteins of cerebral microvessel basal lamina and interendothelial tight junction proteins such as ZO-1, causing BBB disruption and brain edema formation. 23,28 A recent study showed that MMP-9 knockout inhibited post-SAH brain edema formation in mice. 7 Inflammatory cytokines and other factors can regulate the transcription of MMP-9 following SAH.…”

Section: Discussionmentioning

confidence: 99%

“…The time points were selected because previous studies reported that post-SAH BBB disruption peaked within 24 hours and was reversed by 48-72 hours following experimental SAH. 23,29 The brain water content was measured at 24 and 48 hours postsurgery, and BBB permeability and Western blot analyses were evaluated at 24 hours postsurgery (Fig. 1 upper).…”

Section: Subarachnoid Hemorrhage Model and Study Protocolmentioning

confidence: 99%

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Deficiency of tenascin-C and attenuation of blood-brain barrier disruption following experimental subarachnoid hemorrhage in mice

Fujimoto¹,

Shiba²,

Kawakita³

et al. 2016

JNS

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A neurysmAl subarachnoid hemorrhage (SAH) is one of the most life-threatening cerebrovascular disorders, with high mortality and morbidity rates. 26,33 Delayed cerebral ischemia (DCI) remains the most important cause of morbidity and mortality in those patients who survive the initial bleeding. 20 Recent studies have reported that early brain injury (EBI), as well as cerebral vasospasm, is a major cause of DCI following SAH. 20EBI occurs before the onset of cerebral vasospasm and may cause DCI with no significant vasospasm. 3 Brain edema, which results mainly from blood-brain barrier (BBB) disruption, 18 plays an important role in the pathological abbreviatioNs BBB = blood-brain barrier; DCI = delayed cerebral ischemia; EBI = early brain injury; ERK = extracellular signal-regulated kinase; ICA = internal carotid artery; JNK = c-Jun N-terminal kinase; MAPK = mitogen-activated protein kinase; MMP = matrix metalloproteinase; PBS = phosphate-buffered saline; PDGF = plateletderived growth factor; SAH = subarachnoid hemorrhage; TNC = tenascin-C; TNKO = TNC knockout; WT = wild-type; ZO = zona occludens. obJective Tenascin-C (TNC), a matricellular protein, is induced in the brain following subarachnoid hemorrhage (SAH). The authors investigated if TNC causes brain edema and blood-brain barrier (BBB) disruption following experimental SAH. methods C57BL/6 wild-type (WT) or TNC knockout (TNKO) mice were subjected to SAH by endovascular puncture. Ninety-seven mice were randomly allocated to WT sham-operated (n = 16), TNKO sham-operated (n = 16), WT SAH (n = 34), and TNKO SAH (n = 31) groups. Mice were examined by means of neuroscore and brain water content 24-48 hours post-SAH; and Evans blue dye extravasation and Western blotting of TNC, matrix metalloproteinase (MMP)-9, and zona occludens (ZO)-1 at 24 hours post-SAH. As a separate study, 16 mice were randomized to WT sham-operated, TNKO sham-operated, WT SAH, and TNKO SAH groups (n = 4 in each group), and activation of mitogen-activated protein kinases (MAPKs) was immunohistochemically evaluated at 24 hours post-SAH. Moreover, 40 TNKO mice randomly received an intracerebroventricular injection of TNC or phosphate-buffered saline, and effects of exogenous TNC on brain edema and BBB disruption following SAH were studied. results Deficiency of endogenous TNC prevented neurological impairments, brain edema formation, and BBB disruption following SAH; it was also associated with the inhibition of both MMP-9 induction and ZO-1 degradation. Endogenous TNC deficiency also inhibited post-SAH MAPK activation in brain capillary endothelial cells. Exogenous TNC treatment abolished the neuroprotective effects shown in TNKO mice with SAH. coNclusioNs Tenascin-C may be an important mediator in the development of brain edema and BBB disruption following SAH, mechanisms for which may involve MAPK-mediated MMP-9 induction and ZO-1 degradation. TNC could be a molecular target against which to develop new therapies for SAH-induced brain injuries.

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Acute alterations in microvascular basal lamina after subarachnoid hemorrhage

Abstract: Results of this study demonstrated an acute loss of collagen IV from the cerebral microvasculature after SAH and indicated that MMP-9 contributes to this event. The loss of collagen IV might contribute to the known failure of the blood-brain barrier after SAH.

Cited by 117 publications

References 63 publications

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage

Ultrastructural alterations of human cortical capillary basement membrane in human brain oedema

Deficiency of tenascin-C and attenuation of blood-brain barrier disruption following experimental subarachnoid hemorrhage in mice

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