Ontogenic expression of the erythroid-type glucose transporter (Glut 1) in the telencephalon of the mouse: correlation to the tightening of the blood-brain barrier

Bauer, H.; Sonnleitner, U.; Lametschwandtner, Alois; Steiner, Marianne; Adam, Hans; Bauer, Hannelore

doi:10.1016/0165-3806(95)00044-e

Cited by 67 publications

(55 citation statements)

References 35 publications

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“…Its expression accompanies maturation of the blood-brain barrier in the developing brain (38). In the rat brain, Glut-1 expression has been localized to astrocytes, as well as endothelial cells (39).…”

Section: Discussionmentioning

confidence: 99%

Hypoxia and Hypoxia-Inducible Factor-1 Target Genes in Central Nervous System Radiation Injury

Nordal

Nagy

Pintilie

et al. 2004

Clinical Cancer Research

173

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Purpose: Microvascular permeability changes and loss of blood-brain barrier integrity are important features of central nervous system (CNS) radiation injury. Expression of vascular endothelial growth factor (VEGF), an important determinant of microvascular permeability, was examined to assess its role in CNS radiation damage. Because hypoxia mediates VEGF up-regulation through hypoxia-inducible factor-1␣ (HIF1␣) induction, we studied the relationships of hypoxia, HIF1␣ expression, and expression of VEGF in this damage pathway.Experimental Design: Expression of HIF1␣, VEGF, and another hypoxia-responsive gene, glucose transporter-1, was assessed in the irradiated rat spinal cord using immunohistochemistry and in situ hybridization. Hypoxic areas were identified using the nitroimidazole 2-(2-nitro-1H-imidazole-L-yl) -N-(2,2,3,3,3,- Conclusions: VEGF expression appears to play an important role in CNS radiation injury. This focuses attention on VEGF and other genes induced in response to hypoxia as targets for therapy to reduce or prevent CNS radiation damage.

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Section: Discussionmentioning

confidence: 99%

Hypoxia and Hypoxia-Inducible Factor-1 Target Genes in Central Nervous System Radiation Injury

Nordal

Nagy

Pintilie

et al. 2004

Clinical Cancer Research

173

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“…21,25 The GLUT-1 55-kDa isoform, which is expressed in brain microvascular endothelium, was our marker for capillaries. 26,27 GLUT-1 was expressed in capillaries in normal animals and sham-operated control animals. GLUT-1 expression increased in microvessels around infarcts at 2 days, peaking at 7 days after ischemia.…”

Section: Wei Et Al Vascular Changes After Cortical Strokementioning

confidence: 96%

Collateral Growth and Angiogenesis Around Cortical Stroke

Wei

Erinjeri

Rovainen

et al. 2001

Stroke

282

189

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Background and Purpose-We tested the hypothesis that there are significant long-term local vascular changes after ministroke that could form a basis for functional recovery. Methods-A 6-to 8-mm cranial window was opened over the barrel cortex, which was identified by an intrinsic optical signal during mechanical stimulation of the whiskers in anesthetized female Wistar rats. Branches of the middle cerebral artery (MCA) to this region were ligated. Fluorescein isothiocyanate (FITC) transits were recorded by videomicroscopy in each rat just before, immediately after, and 30 days after ligation. Changes in surface vessels and parenchymal perfusion were measured. In similarly prepared rats, angiogenesis was identified by 5-bromo-2-deoxyuridine labeling and immunohistochemistry for the integrin family member ␣ v ␤ 3 . Results-The intrinsic optical signal disappeared immediately after MCA ligations. FITC injection just after ligation demonstrated 3 concentric regions: 1 region of unchanged perfusion, surrounding 1 region of reduced perfusion (the ischemic border) surrounding a central core with little observable perfusion. At 30 days, the following had taken place:(1) diameters and lengths of surface collaterals in the ischemic border had grown significantly, but no new surface vessels were detected, (2) FITC entered occluded MCA segments, (3) arteriocapillary latencies in the ischemic border were shortened compared with latencies just after ligation, and (4) small infarcts were virtually identical to the poorly perfused core. Angiogenesis was confined to the ischemic border. Key Words: cerebral cortex Ⅲ cerebral revascularization Ⅲ microcirclulaton Ⅲ stroke, experimental Ⅲ rats I n the literature on stroke, much attention has been focused on the penumbra. 1 Excitotoxic damage, inflammation, and, ultimately, cell death in the penumbra are possible targets for therapy. 2 Reports from stroke models and patients document the proliferation of vascular cells and expression of markers for angiogenesis surrounding infarcts. [3][4][5][6] Few, if any, new large surface vessels have been found in the brain after stroke, 7 although there is evidence of arteriolar collateral enlargement. 8,9 The relationship between angiogenesis and/or vessel growth and function in the brain after focal ischemia has not been characterized. Conclusions-ArteriolarWithin an hour after creating "ministrokes" in the barrel cortex, there are significant reductions of local cerebral blood flow. 10 The goal of the present study was to evaluate the extent to which perfusion to small regions of ischemia recovers in the functionally identified rat whisker barrel cortex 30 days after ministroke. Specifically, we tested the hypothesis that enlargement and elongation of surface vessels is related to new vessels (angiogenesis) and recovery of flow. If altered surface collaterals can protect ischemic brain from death, they may ultimately support functional neuronal recovery just as angiogenesis may support postischemic myocardial recovery. 11 Normal, ischemic, a...

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“…Studies on developing mammals have indicated that the neuroectodermal microenvironment commits endothelial cells to express barrier properties (Dermietzel et al, 1992;Bauer et al, 1995;Bolz et al, 1996). Concerning GLUT-1 expression in the three-dimensional microvascular pattern exemplified by mammals, this commitment appears to involve all the microvascular elements.…”

Section: Discussionmentioning

confidence: 99%

“…Its subcellular distribution was also quantified (Gerhart et al, 1989;Farrell and Pardridge, 1991). Moreover, the expression of this transporter is developmentally regulated (Dermietzel et al, 1992;Dwyer and Pardridge, 1993;Bauer et al, 1995) and developmental changes in its subcellular distribution have been quantified in embryonic and postnatal brain (Cornford et al, 1993(Cornford et al, , 1994Bolz et al, 1996).…”

mentioning

confidence: 99%

Glucose Transporter Distribution in the Vessels of the Central Nervous System of the Axolotl Ambystoma mexicanum (Urodela: Ambystomatidae)

Lazzari

Bettini

Ciani

2008

The Anatomical Record

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The GLUT-1 isoform of the glucose transporter is commonly considered a reliable molecular marker of blood-brain barrier endothelia in the neural vasculature organized in a three-dimensional network of single vessels. The central nervous system of the axolotl Ambystoma mexicanum is characterized by a vascular architecture that contains both single and paired vessels. The presence and distribution of the GLUT-1 transporter are studied in this urodele using both immunoperoxidase histochemistry and immunogold technique. Light microscopy reveals immunopositivity in both parenchymal and meningeal vessels. The transverse-sectioned pairs of vessels do not show the same size. Furthermore, in the same pair, the two elements often differ in diameter. The main regions of the central nervous system show a different percentage of the paired structures. Only immunogold cytochemistry reveals different staining intensity in the two adjoined elements of a vascular pair. Colloidal gold particles show an asymmetric distribution in the endothelia of both single and paired vessels. These particles are more numerous on the abluminal surface than on the luminal one. The particle density is calculated in both vascular types. The different values could indicate functional differences between single and paired vessels and between the two adjoined elements of a pair, regarding glucose transport.

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Ontogenic expression of the erythroid-type glucose transporter (Glut 1) in the telencephalon of the mouse: correlation to the tightening of the blood-brain barrier

Cited by 67 publications

References 35 publications

Hypoxia and Hypoxia-Inducible Factor-1 Target Genes in Central Nervous System Radiation Injury

Hypoxia and Hypoxia-Inducible Factor-1 Target Genes in Central Nervous System Radiation Injury

Collateral Growth and Angiogenesis Around Cortical Stroke

Glucose Transporter Distribution in the Vessels of the Central Nervous System of the Axolotl Ambystoma mexicanum (Urodela: Ambystomatidae)

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