Structural and Functional Remodeling of the Brain Vasculature Following Stroke

Freitas-Andrade, Moises; Raman‐Nair, Joanna; Lacoste, Baptiste

doi:10.3389/fphys.2020.00948

Cited by 48 publications

(102 citation statements)

References 462 publications

(600 reference statements)

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“…Ischemic stroke induces cortical spreading depressions (CSDs), which are slowly propagating waves of sustained depolarization of neurons and glial cells. CSDs characterized by injured astrocytes can lead to impaired neurovascular coupling in ischemic stroke [ 84 ]. Additionally, in ischemic stroke, astrocytes release 20-HETE to induce vasoconstriction, limiting cerebral blood flow and contributing to the no-reflow phenomena [ 84 , 85 ].…”

Section: Neurovascular Coupling In Ischemic Strokementioning

confidence: 99%

“…This results in a long-lasting increase in capillary resistance that worsens cerebral ischemic injury after stroke [ 90 ]. Loss of pericytes may also exert adverse effects on neurotropic-dependent neuronal survival [ 84 ], which could contribute to neurovascular coupling dysfunction. Conversely, cerebral ischemia can induce metalloproteinase-9 (MMP-9) activation and release in pericytes, which promotes long-term capillary damage and tight-junction breakdown [ 91 ].…”

Section: Neurovascular Coupling In Ischemic Strokementioning

confidence: 99%

“…Caveolae-mediated transcytosis in endothelial cells, which is suppressed under normal conditions to maintain BBB integrity [ 92 ], is activated following ischemic stroke and may contribute to neuroinflammation [ 84 ]. On the other hand, the caveolae of arteriolar endothelial cells (aECs) may play an active role in neurovascular coupling and vasodilation by relaying signals from neurons to cerebral smooth muscle cells [ 93 ].…”

Section: Neurovascular Coupling In Ischemic Strokementioning

confidence: 99%

See 2 more Smart Citations

Novel Mechanistic Insights and Potential Therapeutic Impact of TRPC6 in Neurovascular Coupling and Ischemic Stroke

Shekhar

Liu

Wang

et al. 2021

IJMS

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Ischemic stroke is one of the most disabling diseases and a leading cause of death globally. Despite advances in medical care, the global burden of stroke continues to grow, as no effective treatments to limit or reverse ischemic injury to the brain are available. However, recent preclinical findings have revealed the potential role of transient receptor potential cation 6 (TRPC6) channels as endogenous protectors of neuronal tissue. Activating TRPC6 in various cerebral ischemia models has been found to prevent neuronal death, whereas blocking TRPC6 enhances sensitivity to ischemia. Evidence has shown that Ca2+ influx through TRPC6 activates the cAMP (adenosine 3’,5’-cyclic monophosphate) response element-binding protein (CREB), an important transcription factor linked to neuronal survival. Additionally, TRPC6 activation may counter excitotoxic damage resulting from glutamate release by attenuating the activity of N-methyl-D-aspartate (NMDA) receptors of neurons by posttranslational means. Unresolved though, are the roles of TRPC6 channels in non-neuronal cells, such as astrocytes and endothelial cells. Moreover, TRPC6 channels may have detrimental effects on the blood–brain barrier, although their exact role in neurovascular coupling requires further investigation. This review discusses evidence-based cell-specific aspects of TRPC6 in the brain to assess the potential targets for ischemic stroke management.

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Section: Neurovascular Coupling In Ischemic Strokementioning

confidence: 99%

Section: Neurovascular Coupling In Ischemic Strokementioning

confidence: 99%

Section: Neurovascular Coupling In Ischemic Strokementioning

confidence: 99%

See 1 more Smart Citation

Novel Mechanistic Insights and Potential Therapeutic Impact of TRPC6 in Neurovascular Coupling and Ischemic Stroke

Shekhar

Liu

Wang

et al. 2021

IJMS

View full text Add to dashboard Cite

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“…Angiogenesis and increasing microvessel density following ischemic stroke is associated with neural remodeling and recovery [ 57 ]. Blood vessels may serve as a scaffold to guide newly formed neurons and axons, and functional vessels deliver much needed nutrients and oxygen to supply endogenous repair mechanisms [ 57 , 109 , 110 , 111 ]. The main angiogenic effects of MSC-EVs are believed to be mediated through activation of the NF-κB pathway [ 112 , 113 ].…”

Section: Effect Of Msc Derived Extracellular Vesicles On Neuro-vascular Unit After Strokementioning

confidence: 99%

Mesenchymal Stem Cell Derived Extracellular Vesicles for Repairing the Neurovascular Unit after Ischemic Stroke

Davis

Savitz

Satani

2021

Cells

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Ischemic stroke is a debilitating disease and one of the leading causes of long-term disability. During the early phase after ischemic stroke, the blood-brain barrier (BBB) exhibits increased permeability and disruption, leading to an influx of immune cells and inflammatory molecules that exacerbate the damage to the brain tissue. Mesenchymal stem cells have been investigated as a promising therapy to improve the recovery after ischemic stroke. The therapeutic effects imparted by MSCs are mostly paracrine. Recently, the role of extracellular vesicles released by these MSCs have been studied as possible carriers of information to the brain. This review focuses on the potential of MSC derived EVs to repair the components of the neurovascular unit (NVU) controlling the BBB, in order to promote overall recovery from stroke. Here, we review the techniques for increasing the effectiveness of MSC-based therapeutics, such as improved homing capabilities, bioengineering protein expression, modified culture conditions, and customizing the contents of EVs. Combining multiple techniques targeting NVU repair may provide the basis for improved future stroke treatment paradigms.

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“…Endothelial cell (EC) dysfunction contributes to brain injury in many pathologic conditions (Grammas et al, 2011 ). Brain angiogenesis can restore the function of the blood-brain barrier (BBB) and promote functional recovery from brain injury (Persidsky et al, 2006 ; Freitas-Andrade et al, 2020 ). Brain microvascular (BM) ECs, a major component of the BBB that maintains brain homeostasis, activates angiogenesis (Ruck et al, 2014 ; Huang et al, 2019 ), and is involved in vascular sprouting and tube formation through interactions with the extracellular matrix (ECM).…”

Section: Introductionmentioning

confidence: 99%

Endothelial Progenitor Cell-Derived Microvesicles Promote Angiogenesis in Rat Brain Microvascular Endothelial Cells In vitro

Zeng

Lei

et al. 2021

Front. Cell. Neurosci.

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Brain microvascular endothelial cells (BMECs) are a major component of the blood-brain barrier that maintains brain homeostasis. Preserving and restoring the normal biological functions of BMECs can reverse or reduce brain injury. Endothelial progenitor cells (EPCs) may promote brain vascular remodeling and restore normal endothelial function. As a novel vehicle for cell-cell communication, microvesicles (MVs) have varied biological functions. The present study investigated the biological effects of EPC-derived MVs (EPC-MVs) on BMECs in vitro. We isolated MVs from the supernatant of EPCs in a serum-depleted medium. BMECs were cultured alone or in the presence of EPC-MVs. BMEC viability and proliferation were evaluated with the Cell Counting Kit-8 and by flow cytometry, and the proangiogenic effect of EPC-MVs on BMECs was assessed with the transwell migration, wound healing, and tube formation assays. Our results showed that EPC-derived MVs labeled with DiI were internalized by cultured BMECs; this enhanced BMEC viability and promoted their proliferation. EPC-MVs also stimulated migration and tube formation in BMECs. These results demonstrate that EPC-derived MVs exert a proangiogenic effect on BMECs, which has potential applications in cell-free therapy for brain injury.

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Structural and Functional Remodeling of the Brain Vasculature Following Stroke

Cited by 48 publications

References 462 publications

Novel Mechanistic Insights and Potential Therapeutic Impact of TRPC6 in Neurovascular Coupling and Ischemic Stroke

Novel Mechanistic Insights and Potential Therapeutic Impact of TRPC6 in Neurovascular Coupling and Ischemic Stroke

Mesenchymal Stem Cell Derived Extracellular Vesicles for Repairing the Neurovascular Unit after Ischemic Stroke

Endothelial Progenitor Cell-Derived Microvesicles Promote Angiogenesis in Rat Brain Microvascular Endothelial Cells In vitro

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