Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment
Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebr...
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| Autor*in: |
Lénárt, Nikolett [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Anmerkung: |
© Lénárt et al. 2015 |
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| Übergeordnetes Werk: |
Enthalten in: Cerebrospinal fluid research - London : BioMed Central, 2004, 12(2015), 1 vom: 17. Juli |
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| Übergeordnetes Werk: |
volume:12 ; year:2015 ; number:1 ; day:17 ; month:07 |
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| DOI / URN: |
10.1186/s12987-015-0013-y |
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SPR029290511 |
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| 245 | 1 | 0 | |a Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment |
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| 520 | |a Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. | ||
| 650 | 4 | |a Apolipoprotein B-100 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Transgenic mouse |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Blood–brain barrier |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Brain endothelial cell |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Pericyte |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Glial cell |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Oxidized low density lipoprotein |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Reactive oxygen species |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Permeability |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Membrane fluidity |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Walter, Fruzsina R |4 aut | |
| 700 | 1 | |a Bocsik, Alexandra |4 aut | |
| 700 | 1 | |a Sántha, Petra |4 aut | |
| 700 | 1 | |a Tóth, Melinda E |4 aut | |
| 700 | 1 | |a Harazin, András |4 aut | |
| 700 | 1 | |a Tóth, Andrea E |4 aut | |
| 700 | 1 | |a Vizler, Csaba |4 aut | |
| 700 | 1 | |a Török, Zsolt |4 aut | |
| 700 | 1 | |a Pilbat, Ana-Maria |4 aut | |
| 700 | 1 | |a Vígh, László |4 aut | |
| 700 | 1 | |a Puskás, László G |4 aut | |
| 700 | 1 | |a Sántha, Miklós |4 aut | |
| 700 | 1 | |a Deli, Mária A |4 aut | |
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10.1186/s12987-015-0013-y doi (DE-627)SPR029290511 (SPR)s12987-015-0013-y-e DE-627 ger DE-627 rakwb eng Lénárt, Nikolett verfasserin aut Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lénárt et al. 2015 Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. Apolipoprotein B-100 (dpeaa)DE-He213 Transgenic mouse (dpeaa)DE-He213 Blood–brain barrier (dpeaa)DE-He213 Brain endothelial cell (dpeaa)DE-He213 Pericyte (dpeaa)DE-He213 Glial cell (dpeaa)DE-He213 Oxidized low density lipoprotein (dpeaa)DE-He213 Reactive oxygen species (dpeaa)DE-He213 Permeability (dpeaa)DE-He213 Membrane fluidity (dpeaa)DE-He213 Walter, Fruzsina R aut Bocsik, Alexandra aut Sántha, Petra aut Tóth, Melinda E aut Harazin, András aut Tóth, Andrea E aut Vizler, Csaba aut Török, Zsolt aut Pilbat, Ana-Maria aut Vígh, László aut Puskás, László G aut Sántha, Miklós aut Deli, Mária A aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 12(2015), 1 vom: 17. Juli (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:12 year:2015 number:1 day:17 month:07 https://dx.doi.org/10.1186/s12987-015-0013-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_2003 AR 12 2015 1 17 07 |
| spelling |
10.1186/s12987-015-0013-y doi (DE-627)SPR029290511 (SPR)s12987-015-0013-y-e DE-627 ger DE-627 rakwb eng Lénárt, Nikolett verfasserin aut Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lénárt et al. 2015 Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. Apolipoprotein B-100 (dpeaa)DE-He213 Transgenic mouse (dpeaa)DE-He213 Blood–brain barrier (dpeaa)DE-He213 Brain endothelial cell (dpeaa)DE-He213 Pericyte (dpeaa)DE-He213 Glial cell (dpeaa)DE-He213 Oxidized low density lipoprotein (dpeaa)DE-He213 Reactive oxygen species (dpeaa)DE-He213 Permeability (dpeaa)DE-He213 Membrane fluidity (dpeaa)DE-He213 Walter, Fruzsina R aut Bocsik, Alexandra aut Sántha, Petra aut Tóth, Melinda E aut Harazin, András aut Tóth, Andrea E aut Vizler, Csaba aut Török, Zsolt aut Pilbat, Ana-Maria aut Vígh, László aut Puskás, László G aut Sántha, Miklós aut Deli, Mária A aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 12(2015), 1 vom: 17. Juli (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:12 year:2015 number:1 day:17 month:07 https://dx.doi.org/10.1186/s12987-015-0013-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_2003 AR 12 2015 1 17 07 |
| allfields_unstemmed |
10.1186/s12987-015-0013-y doi (DE-627)SPR029290511 (SPR)s12987-015-0013-y-e DE-627 ger DE-627 rakwb eng Lénárt, Nikolett verfasserin aut Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lénárt et al. 2015 Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. Apolipoprotein B-100 (dpeaa)DE-He213 Transgenic mouse (dpeaa)DE-He213 Blood–brain barrier (dpeaa)DE-He213 Brain endothelial cell (dpeaa)DE-He213 Pericyte (dpeaa)DE-He213 Glial cell (dpeaa)DE-He213 Oxidized low density lipoprotein (dpeaa)DE-He213 Reactive oxygen species (dpeaa)DE-He213 Permeability (dpeaa)DE-He213 Membrane fluidity (dpeaa)DE-He213 Walter, Fruzsina R aut Bocsik, Alexandra aut Sántha, Petra aut Tóth, Melinda E aut Harazin, András aut Tóth, Andrea E aut Vizler, Csaba aut Török, Zsolt aut Pilbat, Ana-Maria aut Vígh, László aut Puskás, László G aut Sántha, Miklós aut Deli, Mária A aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 12(2015), 1 vom: 17. Juli (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:12 year:2015 number:1 day:17 month:07 https://dx.doi.org/10.1186/s12987-015-0013-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_2003 AR 12 2015 1 17 07 |
| allfieldsGer |
10.1186/s12987-015-0013-y doi (DE-627)SPR029290511 (SPR)s12987-015-0013-y-e DE-627 ger DE-627 rakwb eng Lénárt, Nikolett verfasserin aut Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lénárt et al. 2015 Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. Apolipoprotein B-100 (dpeaa)DE-He213 Transgenic mouse (dpeaa)DE-He213 Blood–brain barrier (dpeaa)DE-He213 Brain endothelial cell (dpeaa)DE-He213 Pericyte (dpeaa)DE-He213 Glial cell (dpeaa)DE-He213 Oxidized low density lipoprotein (dpeaa)DE-He213 Reactive oxygen species (dpeaa)DE-He213 Permeability (dpeaa)DE-He213 Membrane fluidity (dpeaa)DE-He213 Walter, Fruzsina R aut Bocsik, Alexandra aut Sántha, Petra aut Tóth, Melinda E aut Harazin, András aut Tóth, Andrea E aut Vizler, Csaba aut Török, Zsolt aut Pilbat, Ana-Maria aut Vígh, László aut Puskás, László G aut Sántha, Miklós aut Deli, Mária A aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 12(2015), 1 vom: 17. Juli (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:12 year:2015 number:1 day:17 month:07 https://dx.doi.org/10.1186/s12987-015-0013-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_2003 AR 12 2015 1 17 07 |
| allfieldsSound |
10.1186/s12987-015-0013-y doi (DE-627)SPR029290511 (SPR)s12987-015-0013-y-e DE-627 ger DE-627 rakwb eng Lénárt, Nikolett verfasserin aut Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Lénárt et al. 2015 Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. Apolipoprotein B-100 (dpeaa)DE-He213 Transgenic mouse (dpeaa)DE-He213 Blood–brain barrier (dpeaa)DE-He213 Brain endothelial cell (dpeaa)DE-He213 Pericyte (dpeaa)DE-He213 Glial cell (dpeaa)DE-He213 Oxidized low density lipoprotein (dpeaa)DE-He213 Reactive oxygen species (dpeaa)DE-He213 Permeability (dpeaa)DE-He213 Membrane fluidity (dpeaa)DE-He213 Walter, Fruzsina R aut Bocsik, Alexandra aut Sántha, Petra aut Tóth, Melinda E aut Harazin, András aut Tóth, Andrea E aut Vizler, Csaba aut Török, Zsolt aut Pilbat, Ana-Maria aut Vígh, László aut Puskás, László G aut Sántha, Miklós aut Deli, Mária A aut Enthalten in Cerebrospinal fluid research London : BioMed Central, 2004 12(2015), 1 vom: 17. Juli (DE-627)476171717 (DE-600)2171132-X 1743-8454 nnns volume:12 year:2015 number:1 day:17 month:07 https://dx.doi.org/10.1186/s12987-015-0013-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_2003 AR 12 2015 1 17 07 |
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Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. 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Lénárt, Nikolett misc Apolipoprotein B-100 misc Transgenic mouse misc Blood–brain barrier misc Brain endothelial cell misc Pericyte misc Glial cell misc Oxidized low density lipoprotein misc Reactive oxygen species misc Permeability misc Membrane fluidity Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment |
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Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment Apolipoprotein B-100 (dpeaa)DE-He213 Transgenic mouse (dpeaa)DE-He213 Blood–brain barrier (dpeaa)DE-He213 Brain endothelial cell (dpeaa)DE-He213 Pericyte (dpeaa)DE-He213 Glial cell (dpeaa)DE-He213 Oxidized low density lipoprotein (dpeaa)DE-He213 Reactive oxygen species (dpeaa)DE-He213 Permeability (dpeaa)DE-He213 Membrane fluidity (dpeaa)DE-He213 |
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Lénárt, Nikolett Walter, Fruzsina R Bocsik, Alexandra Sántha, Petra Tóth, Melinda E Harazin, András Tóth, Andrea E Vizler, Csaba Török, Zsolt Pilbat, Ana-Maria Vígh, László Puskás, László G Sántha, Miklós Deli, Mária A |
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cultured cells of the blood–brain barrier from apolipoprotein b-100 transgenic mice: effects of oxidized low-density lipoprotein treatment |
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Cultured cells of the blood–brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment |
| abstract |
Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. © Lénárt et al. 2015 |
| abstractGer |
Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. © Lénárt et al. 2015 |
| abstract_unstemmed |
Background The apolipoprotein B-100 (ApoB-100) transgenic mouse line is a model of human atherosclerosis. Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. The membrane fluidity changes in ApoB-100 transgenic cells related to brain microvasculature indicate alterations in lipid composition which may be linked to the partial protection against oxLDL toxicity. © Lénárt et al. 2015 |
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Walter, Fruzsina R Bocsik, Alexandra Sántha, Petra Tóth, Melinda E Harazin, András Tóth, Andrea E Vizler, Csaba Török, Zsolt Pilbat, Ana-Maria Vígh, László Puskás, László G Sántha, Miklós Deli, Mária A |
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Latest findings suggest the importance of ApoB-100 in the development of neurodegenerative diseases and microvascular/perivascular localization of ApoB-100 protein was demonstrated in the cerebral cortex of ApoB-100 transgenic mice. The aim of the study was to characterize cultured brain endothelial cells, pericytes and glial cells from wild-type and ApoB-100 transgenic mice and to study the effect of oxidized low-density lipoprotein (oxLDL) on these cells. Methods Morphology of cells isolated from brains of wild type and ApoB-100 transgenic mice was characterized by immunohistochemistry and the intensity of immunolabeling was quantified by image analysis. Toxicity of oxLDL treatment was monitored by real-time impedance measurement and lactate dehydrogenase release. Reactive oxygen species and nitric oxide production, barrier permeability in triple co-culture blood–brain barrier model and membrane fluidity were also determined after low-density lipoprotein (LDL) or oxLDL treatment. Results The presence of ApoB-100 was confirmed in brain endothelial cells, while no morphological change was observed between wild type and transgenic cells. Oxidized but not native LDL exerted dose-dependent toxicity in all three cell types, induced barrier dysfunction and increased reactive oxygen species (ROS) production in both genotypes. A partial protection from oxLDL toxicity was seen in brain endothelial and glial cells from ApoB-100 transgenic mice. Increased membrane rigidity was measured in brain endothelial cells from ApoB-100 transgenic mice and in LDL or oxLDL treated wild type cells. Conclusion The morphological and functional properties of cultured brain endothelial cells, pericytes and glial cells from ApoB-100 transgenic mice were characterized and compared to wild type cells for the first time. 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