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We are analyzing https://link.springer.com/article/10.1186/1750-1326-5-32.

Title:
Pericyte-specific expression of PDGF beta receptor in mouse models with normal and deficient PDGF beta receptor signaling | Molecular Neurodegeneration
Description:
Background Pericytes are integral members of the neurovascular unit. Using mouse models lacking endothelial-secreted platelet derived growth factor-B (PDGF-B) or platelet derived growth factor receptor beta (PDGFRβ) on pericytes, it has been demonstrated that PDGF-B/PDGFRβ interactions mediate pericyte recruitment to the vessel wall in the embryonic brain regulating the development of the cerebral microcirculation and the blood-brain barrier (BBB). Relatively little is known, however, about the roles of PDGF-B/PDGFRβ interactions and pericytes in the adult brain in part due to a lack of adequate and/or properly characterized experimental models. To address whether genetic disruption of PDGFRβ signaling would result in a pericyte-specific insult in adult mice, we studied the pattern and cellular distribution of PDGFRβ expression in the brain in adult control mice and F7 mice that express two hypomorphic Pdgfrβ alleles containing seven point mutations in the cytoplasmic domain of PDGFRβ that impair downstream PDGFRβ receptor signaling. Results Using dual fluorescent in situ hybridization, immunofluorescent staining for different cell types in the neurovascular unit, and a fluorescent in situ proximity ligation assay to visualize molecular PDGF-B/PDGFRβ interactions on brain tissue sections, we show for the first time that PDGFRβ is exclusively expressed in pericytes, and not in neurons, astrocytes or endothelial cells, in the adult brain of control 129S1/SvlmJ mice. PDGFRβ co-localized only with well-established pericyte markers such as Chondroitin Sulfate Proteoglycan NG2 and the xLacZ4 transgenic reporter. We next confirm pericyte-specific PDGFRβ expression in the brains of F7 mutants and show that these mice are viable in spite of substantial 40-60% reductions in regional pericyte coverage of brain capillaries. Conclusions Our data show that PDGFRβ is exclusively expressed in pericytes in the adult 129S1/Sv1mJ and F7 mouse brain. Moreover, our findings suggest that genetic disruption of PDGFRβ signaling results in a pericyte-specific insult in adult F7 mutants and will not exert a primary effect on neurons because PDGFRβ is not expressed in neurons of the adult 129S1/SvlmJ and F7 mouse brain. Therefore, mouse models with normal and deficient PDGFRβ signaling on a 129S1/SvlmJ background may effectively be used to deduce the specific roles of pericytes in maintaining the cerebral microcirculation and BBB integrity in the adult and aging brain as well as during neurodegenerative and brain vascular disorders.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Education
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What CMS is link.springer.com built with?

Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

brain, pdgfrβ, mouse, pericytes, pubmed, mice, article, adult, ssvlmj, google, scholar, pericyte, sections, cas, expression, cells, figure, month, cortex, incubated, control, neurons, signaling, fluorescent, capillaries, background, genetic, lectinpositive, neuronal, igg, staining, cell, expressed, coverage, immunodetection, pdgf, imaging, analysis, interactions, parietal, receptor, confocal, pdgfbpdgfrβ, situ, immunofluorescent, vascular, central, perivascular, hippocampus, green,

Topics {✒️}

nestin-cre+pdgfrβflox/flox transgenic mice platelet-derived growth factor-bb biotin-conjugated lycopersicon esculentum platelet-derived growth factor mouse anti-β-galactosidase igg platlet-derived growth factor open access article nestin-cre transgenic system goat anti-mouse pdgfrβ rabbit anti-human pdgf nestin-cre genetic manipulation b-type pdgf receptor beta-receptors activate unique mouse anti-mouse neun mouse anti-mouse gfap g-protein signaling-5 induction article download pdf control 129s1/svlmj mouse /cgi-bin/exonarraywebsite/plot_selector_cahoy bright-field imaging analysis mouse anti-mouse smi-32 plcγ-dependent downstream signaling endothelial-mural cell signaling pericyte-specific lacz transgene 129s1/svlmj littermate control plcγ-dependent signal transduction adult control 129s1/svlmj lectin-positive brain capillaries human recombinant pdgf-bb 129s1/svlmj genetic background lectin-positive brain microvessels control 129s1/svlmj mice 129s1/svlmj control mice β-gal nuclear immunodetection desmin-positive pericyte coverage graph-pad prism software abundant pericyte-specific marker lectin-positive fluorescent signals endothelial-specific glut1 immunostaining recombinant murine pdgf-bb s100 calcium-binding protein baron-van evercooren ab adjacent endothelial cells proximity ligation experiments endothelial-specific glut1 immunodetection pdgfrβ-positive pericyte coverage 129s1/svlmj littermate controls exact=1&gene=pdgfrb] zheng astrocyte-specific markers glut1-positive brain capillaries

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Schema {🗺️}

WebPage:
      mainEntity:
         headline:Pericyte-specific expression of PDGF beta receptor in mouse models with normal and deficient PDGF beta receptor signaling
         description:Pericytes are integral members of the neurovascular unit. Using mouse models lacking endothelial-secreted platelet derived growth factor-B (PDGF-B) or platelet derived growth factor receptor beta (PDGFRβ) on pericytes, it has been demonstrated that PDGF-B/PDGFRβ interactions mediate pericyte recruitment to the vessel wall in the embryonic brain regulating the development of the cerebral microcirculation and the blood-brain barrier (BBB). Relatively little is known, however, about the roles of PDGF-B/PDGFRβ interactions and pericytes in the adult brain in part due to a lack of adequate and/or properly characterized experimental models. To address whether genetic disruption of PDGFRβ signaling would result in a pericyte-specific insult in adult mice, we studied the pattern and cellular distribution of PDGFRβ expression in the brain in adult control mice and F7 mice that express two hypomorphic Pdgfrβ alleles containing seven point mutations in the cytoplasmic domain of PDGFRβ that impair downstream PDGFRβ receptor signaling. Using dual fluorescent in situ hybridization, immunofluorescent staining for different cell types in the neurovascular unit, and a fluorescent in situ proximity ligation assay to visualize molecular PDGF-B/PDGFRβ interactions on brain tissue sections, we show for the first time that PDGFRβ is exclusively expressed in pericytes, and not in neurons, astrocytes or endothelial cells, in the adult brain of control 129S1/SvlmJ mice. PDGFRβ co-localized only with well-established pericyte markers such as Chondroitin Sulfate Proteoglycan NG2 and the xLacZ4 transgenic reporter. We next confirm pericyte-specific PDGFRβ expression in the brains of F7 mutants and show that these mice are viable in spite of substantial 40-60% reductions in regional pericyte coverage of brain capillaries. Our data show that PDGFRβ is exclusively expressed in pericytes in the adult 129S1/Sv1mJ and F7 mouse brain. Moreover, our findings suggest that genetic disruption of PDGFRβ signaling results in a pericyte-specific insult in adult F7 mutants and will not exert a primary effect on neurons because PDGFRβ is not expressed in neurons of the adult 129S1/SvlmJ and F7 mouse brain. Therefore, mouse models with normal and deficient PDGFRβ signaling on a 129S1/SvlmJ background may effectively be used to deduce the specific roles of pericytes in maintaining the cerebral microcirculation and BBB integrity in the adult and aging brain as well as during neurodegenerative and brain vascular disorders.
         datePublished:2010-08-25T00:00:00Z
         dateModified:2010-08-25T00:00:00Z
         pageStart:1
         pageEnd:11
         license:https://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1750-1326-5-32
         keywords:
            Proximity Ligation Assay
            Pericyte Coverage
            Brain Pericytes
            Proximity Ligation Assay Probe
            Lycopersicon Esculentum Lectin
            Neurosciences
            Neurology
            Molecular Medicine
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         isPartOf:
            name:Molecular Neurodegeneration
            issn:
               1750-1326
            volumeNumber:5
            type:
               Periodical
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         publisher:
            name:BioMed Central
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               name:Ethan A Winkler
               affiliation:
                     name:University of Rochester
                     address:
                        name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Robert D Bell
               affiliation:
                     name:University of Rochester
                     address:
                        name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
                        type:PostalAddress
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               name:Berislav V Zlokovic
               affiliation:
                     name:University of Rochester
                     address:
                        name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
                        type:PostalAddress
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ScholarlyArticle:
      headline:Pericyte-specific expression of PDGF beta receptor in mouse models with normal and deficient PDGF beta receptor signaling
      description:Pericytes are integral members of the neurovascular unit. Using mouse models lacking endothelial-secreted platelet derived growth factor-B (PDGF-B) or platelet derived growth factor receptor beta (PDGFRβ) on pericytes, it has been demonstrated that PDGF-B/PDGFRβ interactions mediate pericyte recruitment to the vessel wall in the embryonic brain regulating the development of the cerebral microcirculation and the blood-brain barrier (BBB). Relatively little is known, however, about the roles of PDGF-B/PDGFRβ interactions and pericytes in the adult brain in part due to a lack of adequate and/or properly characterized experimental models. To address whether genetic disruption of PDGFRβ signaling would result in a pericyte-specific insult in adult mice, we studied the pattern and cellular distribution of PDGFRβ expression in the brain in adult control mice and F7 mice that express two hypomorphic Pdgfrβ alleles containing seven point mutations in the cytoplasmic domain of PDGFRβ that impair downstream PDGFRβ receptor signaling. Using dual fluorescent in situ hybridization, immunofluorescent staining for different cell types in the neurovascular unit, and a fluorescent in situ proximity ligation assay to visualize molecular PDGF-B/PDGFRβ interactions on brain tissue sections, we show for the first time that PDGFRβ is exclusively expressed in pericytes, and not in neurons, astrocytes or endothelial cells, in the adult brain of control 129S1/SvlmJ mice. PDGFRβ co-localized only with well-established pericyte markers such as Chondroitin Sulfate Proteoglycan NG2 and the xLacZ4 transgenic reporter. We next confirm pericyte-specific PDGFRβ expression in the brains of F7 mutants and show that these mice are viable in spite of substantial 40-60% reductions in regional pericyte coverage of brain capillaries. Our data show that PDGFRβ is exclusively expressed in pericytes in the adult 129S1/Sv1mJ and F7 mouse brain. Moreover, our findings suggest that genetic disruption of PDGFRβ signaling results in a pericyte-specific insult in adult F7 mutants and will not exert a primary effect on neurons because PDGFRβ is not expressed in neurons of the adult 129S1/SvlmJ and F7 mouse brain. Therefore, mouse models with normal and deficient PDGFRβ signaling on a 129S1/SvlmJ background may effectively be used to deduce the specific roles of pericytes in maintaining the cerebral microcirculation and BBB integrity in the adult and aging brain as well as during neurodegenerative and brain vascular disorders.
      datePublished:2010-08-25T00:00:00Z
      dateModified:2010-08-25T00:00:00Z
      pageStart:1
      pageEnd:11
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1750-1326-5-32
      keywords:
         Proximity Ligation Assay
         Pericyte Coverage
         Brain Pericytes
         Proximity Ligation Assay Probe
         Lycopersicon Esculentum Lectin
         Neurosciences
         Neurology
         Molecular Medicine
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         name:Molecular Neurodegeneration
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            1750-1326
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            Periodical
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         name:BioMed Central
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            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
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      author:
            name:Ethan A Winkler
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                  name:University of Rochester
                  address:
                     name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Robert D Bell
            affiliation:
                  name:University of Rochester
                  address:
                     name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Berislav V Zlokovic
            affiliation:
                  name:University of Rochester
                  address:
                     name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
                     type:PostalAddress
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      name:University of Rochester
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         name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
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      address:
         name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
         type:PostalAddress
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         name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
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      name:Ethan A Winkler
      affiliation:
            name:University of Rochester
            address:
               name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
               type:PostalAddress
            type:Organization
      name:Robert D Bell
      affiliation:
            name:University of Rochester
            address:
               name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
               type:PostalAddress
            type:Organization
      name:Berislav V Zlokovic
      affiliation:
            name:University of Rochester
            address:
               name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
      name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA
      name:Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, USA

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