Critical role of microvasculature basal lamina in ischemic brain injury

Wang, Chen Xu; Shuaib, Ashfaq

doi:10.1016/j.pneurobio.2007.07.006

Cited by 96 publications

(78 citation statements)

References 88 publications

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“…40 Within 10 minutes of reperfusion, there is evidence of basal lamina degradation and BBB disruption. 41,42 In humans, early opening of the BBB has been documented within 2 to 6 hours (median 3.8 hours) of stroke onset. 21,43 The early disruption of the BBB in stroke may not be uniform over time.…”

Section: Early and Delayed Hemorrhagic Transformationmentioning

confidence: 99%

“…73 Matrix metalloproteinase actions on the basal lamina (e.g., collagen IV, fibronectin, and laminin) could disrupt the endothelial-pericyte-astrocyte complex and facilitate BBB injury and promote HT. 41 The role of TJPs in early HT is unclear since one study found intact TJPs at 24 hours after stroke 74 whereas a human study found increased blood levels of TJPs to be predictive of HT. 75 Early Hemorrhagic Transformation: Role of Other Leukocyte Factors Though leukocyte-derived MMPs appear to be one mediator of early HT, additional leukocyte-derived molecules have been implicated.…”

Section: Early and Delayed Hemorrhagic Transformationmentioning

confidence: 99%

“…90,91 This delayed and prolonged BBB opening is mediated predominantly by brainderived MMPs (MMP-9, MMP-2, and MMP-3), other brain proteases (plasmin, endogenous tPA, urokinase, and cathepsins), 41 neuroinflammation, as well as vascular remodeling and neovascularization. We propose that HT that occurs beyond 18 to 24 hours after ischemic stroke (delayed HT) occurs mostly due to the processes involved in delayed BBB opening after stroke (Figure 3).…”

Section: Delayed Hemorrhagic Transformationmentioning

confidence: 99%

“…In addition, other proteases derived from brain cells also contribute to delayed HT, including MMP-10, MMP-13, MMP-14, TNF-a converting enzyme, plasmins (tPA and urokinase), and cathepsins. 32,34,38,41,56,81 Several brain cells including astrocytes, neurons, microglia, and endothelium can express MMP-9 and have been found to be MMP-9 immunoreactive after stroke. The expression of MMP-9 may vary by severity of ischemia and time from stroke onset.…”

Section: Delayed Hemorrhagic Transformationmentioning

confidence: 99%

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Hemorrhagic Transformation after Ischemic Stroke in Animals and Humans

Jickling

Liu

Stamova

et al. 2013

J Cereb Blood Flow Metab

450

369

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Hemorrhagic transformation (HT) is a common complication of ischemic stroke that is exacerbated by thrombolytic therapy. Methods to better prevent, predict, and treat HT are needed. In this review, we summarize studies of HT in both animals and humans. We propose that early HT (o18 to 24 hours after stroke onset) relates to leukocyte-derived matrix metalloproteinase-9 (MMP-9) and brain-derived MMP-2 that damage the neurovascular unit and promote blood-brain barrier (BBB) disruption. This contrasts to delayed HT (418 to 24 hours after stroke) that relates to ischemia activation of brain proteases (MMP-2, MMP-3, MMP-9, and endogenous tissue plasminogen activator), neuroinflammation, and factors that promote vascular remodeling (vascular endothelial growth factor and high-moblity-group-box-1). Processes that mediate BBB repair and reduce HT risk are discussed, including transforming growth factor beta signaling in monocytes, Src kinase signaling, MMP inhibitors, and inhibitors of reactive oxygen species. Finally, clinical features associated with HT in patients with stroke are reviewed, including approaches to predict HT by clinical factors, brain imaging, and blood biomarkers. Though remarkable advances in our understanding of HT have been made, additional efforts are needed to translate these discoveries to the clinic and reduce the impact of HT on patients with ischemic stroke.

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Section: Early and Delayed Hemorrhagic Transformationmentioning

confidence: 99%

Section: Early and Delayed Hemorrhagic Transformationmentioning

confidence: 99%

Section: Delayed Hemorrhagic Transformationmentioning

confidence: 99%

Section: Delayed Hemorrhagic Transformationmentioning

confidence: 99%

See 2 more Smart Citations

Hemorrhagic Transformation after Ischemic Stroke in Animals and Humans

Jickling

Liu

Stamova

et al. 2013

J Cereb Blood Flow Metab

450

369

View full text Add to dashboard Cite

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“…Hypoperfusion may enhance neutrophil adhesion and inflammation. This first phase of the biphasic permeability, with duration of 3-8 hours after reperfusion, has been attributed to increased inflammatory and oxidative stress on the BBB, in conjunction with enzymatic degradation (MMP-9) of the ECM [62,63]. The no-reflow effect appears more significant with extended periods of ischemia or if the ischemia is associated with venous obstruction.…”

Section: The Mechanisms Of Bbb Disruption During Ischemic Strokementioning

confidence: 99%

Blood-Brain Barrier Disruption During Acute Ischemic Stroke - The Role of Matrix Metalloproteinases and Tight Junctions Proteins

Dulamea¹

2014

JTMR

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Ischemic stroke is a major cause of death and disability worldwide. Intravenous administration of recombinant tissue plasminogen activator (rtPA) is the only approved pharmacological therapy for patients with acute ischemic stroke. Treatment with intravenous rtPA is associated with increased rates of intracranial hemorrhage. This review discusses recent findings about the changes of the components of neurovascular unit and the alteration of blood-brain barrier during stroke. The analysis provide information in order to identify factors with predictive value for hemorrhagic transformation of ischemic stroke both within or after the thrombolysis time window.

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