Vascular Neural Network Phenotypic Transformation After Traumatic Injury: Potential Role in Long-Term Sequelae

Badaut, Jérôme; Bix, Gregory

doi:10.1007/s12975-013-0304-z

Cited by 45 publications

(27 citation statements)

References 128 publications

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“…Pericytes are nearly completely embraced in the basal lamina and actively participate in the formation and degradation of extracellular matrix (ECM) proteins in the basal lamina. On one hand, pericytes produce degrading proteases, including matrix metalloproteinase (MMP)-2 and MMP-9 [27], to enhance ECM degradation in the early stage of angiogenesis [10]. MMP production also enables pericytes to detach from basal lamina and migrate to newly formed microvasculature.…”

Section: Physiological Functions Of Pericytes In the Normal Brainmentioning

confidence: 99%

Pericytes in Brain Injury and Repair After Ischemic Stroke

Cai

Liu

Zhao

et al. 2016

Transl. Stroke Res.

146

107

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Pericytes are functional components of the neurovascular unit (NVU). They provide support to other NVU components and maintain normal physiological functions of the blood-brain barrier (BBB). The brain ischemia and reperfusion result in pathological alterations in pericytes. The intimate anatomical and functional interactions between pericytes and other NVU components play pivotal roles in the progression of stroke pathology. In this review, we depict the biology and functions of pericytes in the normal brain and discuss their effects in brain injury and repair after ischemia/reperfusion. Since ischemic stroke occurs mostly in elderly people, we also review age-related changes in pericytes and how these changes predispose aged brains to ischemic/reperfusion injury. Strategies targeting pericytes responses after ischemia and reperfusion may provide new therapies for ischemic stroke.

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Section: Physiological Functions Of Pericytes In the Normal Brainmentioning

confidence: 99%

Pericytes in Brain Injury and Repair After Ischemic Stroke

Cai

Liu

Zhao

et al. 2016

Transl. Stroke Res.

146

107

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“…The intake of small molecules causes the mitochondria to swell and break, which further not only disrupts the energy metabolism and ion homeostasis but also releases caspases and the activators of apoptosis, so triggering caspase-mediated progressive cell death. Caspases hydrolyze proteins severely in injured axons [14–17]. In this way, impairment of the mitochondria, imbalance in ion homeostasis, the release of proapoptotic factors, and activation of caspases are key contributors to the high mortality and poor prognosis of DAI.…”

Section: Pathological Mechanism Of Daimentioning

confidence: 99%

Progress of Research on Diffuse Axonal Injury after Traumatic Brain Injury

Zhang

Wang

et al. 2016

Neural Plasticity

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The current work reviews the concept, pathological mechanism, and process of diagnosing of DAI. The pathological mechanism underlying DAI is complicated, including axonal breakage caused by axonal retraction balls, discontinued protein transport along the axonal axis, calcium influx, and calpain-mediated hydrolysis of structural protein, degradation of axonal cytoskeleton network, the changes of transport proteins such as amyloid precursor protein, and changes of glia cells. Based on the above pathological mechanism, the diagnosis of DAI is usually made using methods such as CT, traditional and new MRI, biochemical markers, and neuropsychological assessment. This review provides a basis in literature for further investigation and discusses the pathological mechanism. It may also facilitate improvement of the accuracy of diagnosis for DAI, which may come to play a critical role in breaking through the bottleneck of the clinical treatment of DAI and improving the survival and quality of life of patients through clear understanding of pathological mechanisms and accurate diagnosis.

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“…Foot-fault and rotarod testing was performed at 1, 3,6,8,12, and 14 days, where the foot-fault test was used to evaluate sensorimotor and proprioception and the rotarod test evaluated sensorimotor coordination as previously reported in our earlier studies. 21 All tests at each time-point were carried out on WT and AQP4 À/À mice within a 3-h morning time-block (8-11 am) and WT and AQP4 À/À were interleaved during the testing sequence.…”

Section: Behavioral Testingmentioning

confidence: 99%

Improved long-term outcome after transient cerebral ischemia in aquaporin-4 knockout mice

Hirt

Fukuda

Ambadipudi

et al. 2016

J Cereb Blood Flow Metab

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A hallmark of stroke is water accumulation (edema) resulting from dysregulation of osmotic homeostasis. Brain edema contributes to tissue demise and may lead to increased intracranial pressure and lethal herniation. Currently, there are only limited treatments to prevent edema formation following stroke. Aquaporin 4 (AQP4), a brain water channel, has become a focus of interest for therapeutic approaches targeting edema. At present, there are no pharmacological tools to block AQP4. The role of AQP4 in edema after brain injury remains unclear with conflicting results from studies using AQP4 À/À mice and of AQP4 expression following stroke. Here, we studied AQP4 and its role in edema formation by testing AQP4À/À mice in a model of middle cerebral artery occlusion using novel quantitative MRI water content measurements, histology and behavioral changes as outcome measures. Absence of AQP4 was associated with decreased mortality and increased motor recovery 3 to 14 days after stroke. Behavioral improvement was associated with decreased lesion volume, neuronal cell death and neuroinflammation in AQP4 À/À compared to wild type mice. Our data suggest that the lack of AQP4 confers an overall beneficial role at long term with improved neuronal survival and reduced neuroinflammation, but without a direct effect on edema formation.

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Vascular Neural Network Phenotypic Transformation After Traumatic Injury: Potential Role in Long-Term Sequelae

Cited by 45 publications

References 128 publications

Pericytes in Brain Injury and Repair After Ischemic Stroke

Pericytes in Brain Injury and Repair After Ischemic Stroke

Progress of Research on Diffuse Axonal Injury after Traumatic Brain Injury

Improved long-term outcome after transient cerebral ischemia in aquaporin-4 knockout mice

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