Expression of drug transporters at the blood–brain barrier using an optimized isolated rat brain microvessel strategy

Yousif, Salah; Marie-Claire, Cynthia; Roux, F.; Scherrmann, Jean‐Michel; Declèves, Xavier

doi:10.1016/j.brainres.2006.11.089

Cited by 127 publications

(140 citation statements)

References 32 publications

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“…Brain microvessels were isolated as described by Yousif et al (2007). We used kidney samples as positive controls for our PCR because this tissue has a high concentration of Octs mRNA.…”

Section: Isolation Of Mouse Brain Microvessels Cortex and Kidney Samentioning

confidence: 99%

Transport of Biogenic Amine Neurotransmitters at the Mouse Blood–Retina and Blood–Brain Barriers by Uptake1 and Uptake2

André

Saubaméa

Cochois-Guégan

et al. 2012

J Cereb Blood Flow Metab

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Uptake1 and uptake2 transporters are involved in the extracellular clearance of biogenic amine neurotransmitters at synaptic clefts. We looked for them at the blood-brain barrier (BBB) and bloodretina barriers (BRB), where they could be involved in regulating the neurotransmitter concentration and modulate/terminate receptor-mediated effects within the neurovascular unit (NVU). Uptake2 (Oct1-3/ Slc22a1-3, Pmat/Slc29a4) and Mate1/Slc47a1 transporters are also involved in the transport of xenobiotics. We used in situ carotid perfusion of prototypic substrates like-serotonin, and [ 3 H]-dopamine, changes in ionic composition and genetic deletion of Oct1-3 carriers to detect uptake1 and uptake2 at the BBB and BRB. We showed that uptake1 and uptake2 are involved in the transport of [ 3 H]-dopamine and [ 3 H]-MPP + at the blood luminal BRB, but not at the BBB. These functional studies, together with quantitative RT-PCR and confocal imaging, suggest that the mouse BBB lacks uptake1 (Net/Slc6a2, Dat/Slc6a3, Sert/Slc6a4), uptake2, and Mate1 on both the luminal and abluminal sides. However, we found evidence for functional Net and Oct1 transporters at the luminal BRB. These heterogeneous transport properties of the brain and retina NVUs suggest that the BBB helps protect the brain against biogenic amine neurotransmitters in the plasma while the BRB has more of a metabolic/endocrine role.

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“…Brain microvessels were isolated as described by Yousif et al (2007). We used kidney samples as positive controls for our PCR because this tissue has a high concentration of Octs mRNA.…”

Section: Isolation Of Mouse Brain Microvessels Cortex and Kidney Samentioning

confidence: 99%

Transport of Biogenic Amine Neurotransmitters at the Mouse Blood–Retina and Blood–Brain Barriers by Uptake1 and Uptake2

André

Saubaméa

Cochois-Guégan

et al. 2012

J Cereb Blood Flow Metab

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“…For microvessel isolation, all procedures were carried out at 41C, as described previously (Yousif et al, 2007). Briefly, freshly dissected cortical tissue, obtained from P21 rats, was homogenized and centrifuged at 1,000 Â g for 10 mins.…”

Section: Tissue Collection and Preparationmentioning

confidence: 99%

Stimulatory Effects of Thyroid Hormone on Brain Angiogenesis in vivo and in vitro

Zhang

Cooper-Kuhn

Nannmark

et al. 2009

J Cereb Blood Flow Metab

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Thyroid hormone is critical for the proper development of the central nervous system. However, the specific role of thyroid hormone on brain angiogenesis remains poorly understood. Treatment of rats from birth to postnatal day 21 (P21) with propylthiouracil (PTU), a reversible blocker of triiodothyronine (T3) synthesis, resulted in decreased brain angiogenesis, as indicated by reduced complexity and density of microvessels. However, when PTU was withdrawn at P22, these parameters were fully recovered by P90. These changes were paralleled by an altered expression of vascular endothelial growth factor A (Vegfa) and basic fibroblast growth factor (Fgf2). Physiologic concentrations of T3 and thyroxine (T4) stimulated proliferation and tubulogenesis of rat brainderived endothelial (RBE4) cells in vitro. Protein and mRNA levels of VEGF-A and FGF-2 increased after T3 stimulation of RBE4 cells. The thyroid hormone receptor blocker NH-3 abolished T3-induced Fgf2 and Vegfa upregulation, indicating a receptor-mediated effect. Thyroid hormone inhibited the apoptosis in RBE4 cells and altered mRNA levels of apoptosis-related genes, namely Bcl2 and Bad. The present results show that thyroid hormone has a substantial impact on vasculature development in the brain. Pathologically altered vascularization could, therefore, be a contributing factor to the neurologic deficits induced by thyroid hormone deficiency.

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“…Rat brain microvessel endothelial cells (rBMECs) were primarily isolated from the cerebral gray matter of rat brains as described previously, 47,48 with minor modifications. In brief, the isolated rat cerebral gray matter was homogenized and filtrated with 145 μm and 70 μm nylon meshes, the matter on the 70 μm nylon mesh was collected and digested with type II collagenase (0.1%) at 37 °C for 30 min, and then centrifuged at room temperature for 10 min (200 × g).…”

Section: Chemicals and Animalsmentioning

confidence: 99%

Synergistic inhibition of angiogenesis and glioma cell-induced angiogenesis by the combination of temozolomide and enediyne antibiotic lidamycin

Ouyang

Zhang

et al. 2014

Cancer Biology & Therapy

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Expression of drug transporters at the blood–brain barrier using an optimized isolated rat brain microvessel strategy

Cited by 127 publications

References 32 publications

Transport of Biogenic Amine Neurotransmitters at the Mouse Blood–Retina and Blood–Brain Barriers by Uptake1 and Uptake2

Transport of Biogenic Amine Neurotransmitters at the Mouse Blood–Retina and Blood–Brain Barriers by Uptake1 and Uptake2

Stimulatory Effects of Thyroid Hormone on Brain Angiogenesis in vivo and in vitro

Synergistic inhibition of angiogenesis and glioma cell-induced angiogenesis by the combination of temozolomide and enediyne antibiotic lidamycin

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