Morphogens and blood-brain barrier function in health and disease

Wevers, Nienke R.; Vries, Helga E. de

doi:10.1080/21688370.2015.1090524

Cited by 38 publications

(27 citation statements)

References 154 publications

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“…Additional intercellular proteins of endothelial cells, such as junction adhesion molecules (JAMs) and platelet/endothelial cell adhesion molecules (PECAMs), actively suppress transendothelial migration of monocytes and neutrophils [167, 168], where a loss of these proteins increases paracellular permeability. The vasculature of the CNS and its transcellular activity is also unique as compared to peripheral nervous system blood vessels [169], where communication between endothelial cells and both astrocytes and pericytes actively maintains BBB integrity [35, 170], thus mitigating transcellular-mediated communication. Here, further insight into the acute molecular mechanisms of BBB disruption is provided at a paracellular and transcellular level following UMEA implantation (Figure 7A).…”

Section: Discussionmentioning

confidence: 99%

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Neuroinflammation, oxidative stress, and blood-brain barrier (BBB) disruption in acute Utah electrode array implants and the effect of deferoxamine as an iron chelator on acute foreign body response

et al. 2019

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The use of intracortical microelectrode arrays has gained significant attention in being able to help restore function in paralysis patients and study the brain in various neurological disorders. Electrode implantation in the cortex causes vasculature or blood-brain barrier (BBB) disruption and thus elicits a foreign body response (FBR) that results in chronic inflammation and may lead to poor electrode performance. In this study, a comprehensive insight into the acute molecular mechanisms occurring at the Utah electrode array-tissue interface is provided to understand the oxidative stress, neuroinflammation, and neurovascular unit (astrocytes, pericytes, and endothelial cells) disruption that occurs following microelectrode implantation. Quantitative real time polymerase chain reaction (qRT-PCR) was used to quantify the gene expression at acute time-points of 48-hr, 72-hr, and 7-days for factors mediating oxidative stress, inflammation, and BBB disruption in rats implanted with a non-functional 4×4 Utah array in the somatosensory cortex. During vascular disruption, free iron released into the brain parenchyma can exacerbate the FBR, leading to oxidative stress and thus further contributing to BBB degradation. To reduce the free iron released into the brain tissue, the effects of an iron chelator, deferoxamine mesylate (DFX), was also evaluated.

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Section: Discussionmentioning

confidence: 99%

“…The neurovascular unit (Figure 7A) consists of neurons, endothelial cells, pericytes, and astrocytes and provides the brain parenchyma with a homeostatic environment [170, 195]. The complete role of pericytes in the CNS is still not fully understood.…”

Section: Discussionmentioning

confidence: 99%

Neuroinflammation, oxidative stress, and blood-brain barrier (BBB) disruption in acute Utah electrode array implants and the effect of deferoxamine as an iron chelator on acute foreign body response

et al. 2019

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“…Another option is to grow a vessel of brain microvascular pericytes and endothelial cells in the medium channel adjacent to the neuronal-glial networks and mimic the blood-brain barrier (BBB)34. The BBB is a highly specialized barrier that ensures a homeostatic environment for the CNS.…”

Section: Discussionmentioning

confidence: 99%

High-throughput compound evaluation on 3D networks of neurons and glia in a microfluidic platform

Wevers

Vught

Wilschut

et al. 2016

Sci Rep

118

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With great advances in the field of in vitro brain modelling, the challenge is now to implement these technologies for development and evaluation of new drug candidates. Here we demonstrate a method for culturing three-dimensional networks of spontaneously active neurons and supporting glial cells in a microfluidic platform. The high-throughput nature of the platform in combination with its compatibility with all standard laboratory equipment allows for parallel evaluation of compound effects.

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“…In MS, upon inflammatory stimulation the BBB itself and its anti-inflammatory function are compromised changed (Wevers and de Vries 2016). It enables the inflammatory cells (T cells, monocytes/macrophages) penetrate the BBB.…”

Section: The Potential Role Of Blood Platelets In Multiple Sclerosismentioning

confidence: 99%

The physiology of blood platelets and changes of their biological activities in multiple sclerosis

Wachowicz¹,

Morel²,

Miller³

et al. 2016

Acta Neurobiologiae Experimentalis

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Increasing evidence indicates that blood platelets contribute to diverse processes that extend beyond hemostasis. Many of the same mechanisms that play a role in hemostasis and thrombosis facilitate platelets the participation in other physiological and pathological processes, particularly in the inflammation, the immune response and central nervous system disorders. Platelets are involved in pathophysiology of central nervous system diseases, especially in the pathogenesis of multiple sclerosis, but their role appears to be neglected. Platelets contribute to the inflammation and cooperate with immune cells in inflammatory and immune responses. These blood cells were identified in inflamed spinal cord and in the brain in chronic active lesions of multiple sclerosis and in the related animal models referred as Experimental Autoimmune Encephalomyelitis. This review summarizes recent insights in the platelet activation accompanied by the exocytosis of bioactive compounds stored in granules, formation of platelet microparticles, expression of specific membrane receptors, synthesis of numerous biomediators, generation of free radicals, and introduces the mechanisms by which activated platelets may be involved in the pathophysiology of multiple sclerosis. Understanding the role of platelets in multiple sclerosis may be essential for improved therapies.

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Morphogens and blood-brain barrier function in health and disease

Cited by 38 publications

References 154 publications

Neuroinflammation, oxidative stress, and blood-brain barrier (BBB) disruption in acute Utah electrode array implants and the effect of deferoxamine as an iron chelator on acute foreign body response

Neuroinflammation, oxidative stress, and blood-brain barrier (BBB) disruption in acute Utah electrode array implants and the effect of deferoxamine as an iron chelator on acute foreign body response

High-throughput compound evaluation on 3D networks of neurons and glia in a microfluidic platform

The physiology of blood platelets and changes of their biological activities in multiple sclerosis

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