Activated Microvessels Express Vascular Endothelial Growth Factor and Integrin α<sub>v</sub>β<sub>3</sub> During Focal Cerebral Ischemia

Abumiya, Takeo; Lucero, Jacinta; Heo, Ji Hoe; Tagaya, Masayoshi; Koziol, James A.; Copeland, Brian R.; Zoppo, Gregory J. del

doi:10.1097/00004647-199909000-00012

Cited by 138 publications

(145 citation statements)

References 54 publications

(65 reference statements)

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“…The cerebral vasculature responds to focal ischemia through changes in the gene expression profile of vascular endothelial cells, including new patterns of cell adhesion molecules, vascular growth factors, and chemokines (Abumiya et al, 1999;Stumm et al, 2002). Our findings show that stroke induces a wave of expression of the chemokine SDF1 and the vascular growth factor Ang1 in peri-infarct blood vessels.…”

Section: Discussionmentioning

confidence: 67%

“…Within degenerating striatum, DCX ϩ cells appear to migrate along both astrocytes and blood vessels (Thored et al, 2006;Yamashita et al, 2006). Stroke alters the molecular profile of endothelial cells in peri-infarct cortex (Abumiya et al, 1999;Stumm et al, 2002), the site of in-migration of neuroblasts after stroke. We hypothesized that stroke changes the cellular environment in peri-infarct cortex by forming a unique neurovascular niche in which newly born neuroblasts associate with vascular endothelial cells.…”

Section: Neuroblasts Associate With Remodeling Blood Vessels In a Neumentioning

confidence: 99%

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A Neurovascular Niche for Neurogenesis after Stroke

Ohab¹,

Fleming²,

Blesch³

et al. 2006

J. Neurosci.

785

783

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Stroke causes cell death but also birth and migration of new neurons within sites of ischemic damage. The cellular environment that induces neuronal regeneration and migration after stroke has not been defined. We have used a model of long-distance migration of newly born neurons from the subventricular zone to cortex after stroke to define the cellular cues that induce neuronal regeneration after CNS injury. Mitotic, genetic, and viral labeling and chemokine/growth factor gain-and loss-of-function studies show that stroke induces neurogenesis from a GFAP-expressing progenitor cell in the subventricular zone and migration of newly born neurons into a unique neurovascular niche in peri-infarct cortex. Within this neurovascular niche, newly born, immature neurons closely associate with the remodeling vasculature. Neurogenesis and angiogenesis are causally linked through vascular production of stromal-derived factor 1 (SDF1) and angiopoietin 1 (Ang1). Furthermore, SDF1 and Ang1 promote post-stroke neuroblast migration and behavioral recovery. These experiments define a novel brain environment for neuronal regeneration after stroke and identify molecular mechanisms that are shared between angiogenesis and neurogenesis during functional recovery from brain injury.

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Section: Discussionmentioning

confidence: 67%

Section: Neuroblasts Associate With Remodeling Blood Vessels In a Neumentioning

confidence: 99%

A Neurovascular Niche for Neurogenesis after Stroke

Ohab¹,

Fleming²,

Blesch³

et al. 2006

J. Neurosci.

785

783

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“…Immunohistochemistry of confluent cells: expression by confluent endothelial cells was demonEndothelial cell claudin-5 depends on matrix adhesion T Osada et al strated by immunoperoxidase or by immunofluorescence methods as required (Abumiya et al, 1999). The impact of b 1 -integrin function blockade on interendothelial claudin-5 expression was determined with the aid of quantitative video-imaging microscopy.…”

Section: Tight Junction Expressionmentioning

confidence: 99%

Interendothelial Claudin-5 Expression Depends on Cerebral Endothelial Cell–Matrix Adhesion by β₁-Integrins

Osada

Kanazawa

et al. 2011

J Cereb Blood Flow Metab

121

120

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The hypothesis tested by these studies states that in addition to interendothelial cell tight junction proteins, matrix adhesion by b 1 -integrin receptors expressed by endothelial cells have an important role in maintaining the cerebral microvessel permeability barrier. Primary brain endothelial cells from C57 BL/6 mice were incubated with b 1 -integrin function-blocking antibody (Ha2/5) or isotype control and the impacts on claudin-5 expression and microvessel permeability were quantified. Both flow cytometry and immunofluorescence studies demonstrated that the interendothelial claudin-5 expression by confluent endothelial cells was significantly decreased in a time-dependent manner by Ha2/5 exposure relative to isotype. Furthermore, to assess the barrier properties, transendothelial electrical resistance and permeability measurements of the monolayer, and stereotaxic injection into the striatum of mice were performed. Ha2/5 incubation reduced the resistance of endothelial cell monolayers significantly, and significantly increased permeability to 40 and 150 kDa dextrans. Ha2/5 injection into mouse striatum produced significantly greater IgG extravasation than the isotype or the control injections. This study demonstrates that blockade of b 1 -integrin function changes interendothelial claudin-5 expression and increases microvessel permeability. Hence, endothelial cell-matrix interactions via b 1 -integrin directly affect interendothelial cell tight junction claudin-5 expression and brain microvascular permeability.

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“…84 But, subunit ␣ 5 , and not ␣ 4 , has been identified on adult human cerebral microvessels in one report. 82…”

Section: Other Integrin Receptors ␣ 4 and ␣ 5 Integrinsmentioning

confidence: 99%

“…32,84 Integrin ␣ v ␤ 3 expression is significantly upregulated after the onset of focal ischemia. 85 …”

Section: Adhesion Receptor Expression In the Adult Brainmentioning

confidence: 99%

Cerebral Microvasculature

2011

Encyclopedia of Clinical Neuropsychology

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Abstract-The integrity of all organ systems requires faithful interaction between its component cells and the extracellular matrix (ECM). In the central nervous system (CNS), matrix adhesion receptors are uniquely expressed by the cells comprising the microvascular compartment, and by neurons and their supporting glial cells. Cells within the cerebral microvasculature express both the integrin and dystroglycan families of matrix adhesion receptors. However, the functional significance of these receptors is only now being explored. Capillaries of the cerebral microvasculature consist of the luminal endothelium, which is separated from circumferential astrocyte end-feet by the intervening ECM of the basal lamina. Endothelial cells and astrocytes cooperate to generate and maintain the basal lamina and the unique barrier functions of the endothelium. Integrins and the dystroglycan complex are found on the matrix-proximate faces of both endothelial cells and astrocyte end-feet. Pericytes rest against the basal lamina. In the extravascular compartment, select integrins are expressed on neurons, microglial cells, and oligodendroglia. Significant alterations in both cellular adhesion receptors and their ligands occur under the conditions of focal cerebral ischemia, multiple sclerosis (MS) and the modeled condition experimental autoimmune encephalomyelitis (EAE), certain tumors of the CNS, and arteriovenous malformations (AVMs). The changes in matrix adhesion receptor expression in these conditions support their functional significance in the normal state. We propose that matrix adhesion receptors are essential for the maintenance of the integrity of the blood-brain permeability barrier, and that modulation of these receptors contribute to alterations in the barrier during brain injury. This review examines current information about cell adhesion receptor expression within the cerebral microvasculature and surrounding tissue, and their potential roles during the vascular responses to local injury. T he cerebral microvasculature is unique in that while serving as a conduit for supplying blood-to-brain structures, it is also completely incorporated within the neuropil, allowing direct interactions with glia and neurons. The cerebral microvasculature is also functionally dynamic. It maintains and with states of arousal and neuronal activation increases local and regional blood flow to provide cellular nutritional support. 1-4 Both local and distant control of cerebral blood flow during activation results from neuronvascular coupling via astrocytes, and from direct innervation. 1,2 The close proximity between the endothelium and astrocyte end-feet of intact cerebral capillaries also implies potential communication between the cells across the basal lamina.Pial and cortical penetrating arteries consist of an endothelial cell layer, the basal lamina (derived from the extracellular matrix [ECM]), a myointima with smooth muscle cells encased in the matrix, and an adventitia. 5 Arising from the leptomeninges, the adventitia of th...

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Activated Microvessels Express Vascular Endothelial Growth Factor and Integrin α_vβ₃ During Focal Cerebral Ischemia

Cited by 138 publications

References 54 publications

A Neurovascular Niche for Neurogenesis after Stroke

A Neurovascular Niche for Neurogenesis after Stroke

Interendothelial Claudin-5 Expression Depends on Cerebral Endothelial Cell–Matrix Adhesion by β₁-Integrins

Cerebral Microvasculature

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Activated Microvessels Express Vascular Endothelial Growth Factor and Integrin αvβ3 During Focal Cerebral Ischemia

Cited by 138 publications

References 54 publications

A Neurovascular Niche for Neurogenesis after Stroke

A Neurovascular Niche for Neurogenesis after Stroke

Interendothelial Claudin-5 Expression Depends on Cerebral Endothelial Cell–Matrix Adhesion by β1-Integrins

Cerebral Microvasculature

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Activated Microvessels Express Vascular Endothelial Growth Factor and Integrin α_vβ₃ During Focal Cerebral Ischemia

Interendothelial Claudin-5 Expression Depends on Cerebral Endothelial Cell–Matrix Adhesion by β₁-Integrins