We are analyzing https://link.springer.com/article/10.1007/s11481-008-9118-2.

Title:
MFG-E8 Regulates Microglial Phagocytosis of Apoptotic Neurons | Journal of Neuroimmune Pharmacology
Description:
Phagocytosis is an essential mechanism for clearance of pathogens, dying cells, and other unwanted debris in order to maintain tissue health in the body. Macrophages execute this process in the peripheral immune system but in the brain microglia act as resident macrophages to accomplish this function. In the peripheral immune system, macrophages secrete Milk Fat Globule Factor-E8 (MFG-E8) that recognizes phosphatidylserine “eat me” signals expressed on the surface of apoptotic cells. MFG-E8 then acts as a tether to attach the apoptotic cell to the macrophage and trigger a signaling cascade that stimulates the phagocyte development, allowing the macrophage to engulf the dying cell. When this process becomes disrupted, inflammation and autoimmunity can result. MFG-E8 resides in the brain as well as in the periphery, and microglia express MFG-E8. However, the function of MFG-E8 in the brain has not been elucidated. We measured MFG-E8 production in the BV-2 microglial cell line and the role of this protein in the recognition and engulfment of apoptotic SY5Y neuroblastoma cells. BV-2 cells produced and released MFG-E8, which apoptotic SY5Y cells and the chemokine fractalkine further stimulated. Furthermore, MFG-E8 increased phagocytosis of apoptotic SY5Y cells, and a dominant negative form of MFG-E8 inhibited phagocytosis by BV-2 cells. Finally, brain MFG-E8 levels were altered in a mouse model of Alzheimer’s disease. Our data suggest that MFG-E8 acts in the brain via microglia to aid in clearance of apoptotic neurons, and we hypothesize that a dysregulation of this process may be involved in neurodegenerative disease.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Education
Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

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

Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We see no obvious way the site makes money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

cells, mfge, apoptotic, cell, phagocytosis, article, microglia, pubmed, google, scholar, cas, syy, fractalkine, brain, protein, production, levels, fig, data, microglial, media, neurons, usa, assay, control, clearance, mice, negative, coculture, system, model, disease, μgml, macrophages, line, treatment, increase, role, increased, receptor, hanayama, mechanism, dominant, mouse, shown, significant, addition, western, bioparticles, immune,

Topics {✒️}

v-raf/v-myc carrying retrovirus horseradish-peroxidase-conjugated secondary antibody factor-viii-homologous domains age-matched wild-type littermates wild-type age-matched littermates silver-stained sds-page gel age-matched wild-type animals fractalkine-induced mfg-e8 leads recombinant wild-type mfg-e8 epidermal growth factor mouse monoclonal anti-β-actin intraneuronal beta-amyloid aggregates growth arrest-specific gene wild-type animals displayed mfg-e8 mrna expression inducible nitric-oxide synthase crkii-dock180-rac1 complex antimouse mfg-e8 antibody anti-mfg-e8 antibody mfg-e8 inhibited phagocytosis inhibit mfg-e8 production recombinant mfg-e8 yields direct cell–cell contact article download pdf recombinant mouse mfg-e8 regulating mfg-e8 production increasing mfg-e8 expression inhibits mfg-e8 production dominant negative mfg-e8 mfg-e8-deficient mice 100 ng/ml mfg-e8 mfg-e8-dependent mechanism mfg-e8 protein production mfg-e8 inhibits phagocytosis mfg-e8-dependent clearance normal mfg-e8 production sterile phosphate-buffered saline mfg-e8 protein levels adding recombinant mfg-e8 mfg-e8 induced confirmed mfg-e8 production implicated mfg-e8 suppressed mfg-e8 levels mfg-e8 levels increased measured mfg-e8 production mfg-e8-mediated phagocytosis inflammatory state induced endogenous mfg-e8 produced stimulated mfg-e8 production brain mfg-e8 production

Questions {❓}

Henson PM, Bratton DL, Fadok VA (2001) The phosphatidylserine receptor: a crucial molecular switch?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:MFG-E8 Regulates Microglial Phagocytosis of Apoptotic Neurons
         description:Phagocytosis is an essential mechanism for clearance of pathogens, dying cells, and other unwanted debris in order to maintain tissue health in the body. Macrophages execute this process in the peripheral immune system but in the brain microglia act as resident macrophages to accomplish this function. In the peripheral immune system, macrophages secrete Milk Fat Globule Factor-E8 (MFG-E8) that recognizes phosphatidylserine “eat me” signals expressed on the surface of apoptotic cells. MFG-E8 then acts as a tether to attach the apoptotic cell to the macrophage and trigger a signaling cascade that stimulates the phagocyte development, allowing the macrophage to engulf the dying cell. When this process becomes disrupted, inflammation and autoimmunity can result. MFG-E8 resides in the brain as well as in the periphery, and microglia express MFG-E8. However, the function of MFG-E8 in the brain has not been elucidated. We measured MFG-E8 production in the BV-2 microglial cell line and the role of this protein in the recognition and engulfment of apoptotic SY5Y neuroblastoma cells. BV-2 cells produced and released MFG-E8, which apoptotic SY5Y cells and the chemokine fractalkine further stimulated. Furthermore, MFG-E8 increased phagocytosis of apoptotic SY5Y cells, and a dominant negative form of MFG-E8 inhibited phagocytosis by BV-2 cells. Finally, brain MFG-E8 levels were altered in a mouse model of Alzheimer’s disease. Our data suggest that MFG-E8 acts in the brain via microglia to aid in clearance of apoptotic neurons, and we hypothesize that a dysregulation of this process may be involved in neurodegenerative disease.
         datePublished:2008-08-01T00:00:00Z
         dateModified:2008-08-01T00:00:00Z
         pageStart:246
         pageEnd:256
         license:https://creativecommons.org/licenses/by-nc/2.0
         sameAs:https://doi.org/10.1007/s11481-008-9118-2
         keywords:
            MFG-E8
            microglia
            phagocytosis
            apoptosis
            fractalkine
            Alzheimer’s disease
            Neurosciences
            Immunology
            Pharmacology/Toxicology
            Virology
            Cell Biology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig5_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig6_HTML.gif
         isPartOf:
            name:Journal of Neuroimmune Pharmacology
            issn:
               1557-1904
               1557-1890
            volumeNumber:3
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Abby D. Fuller
               affiliation:
                     name:Northwestern University Feinberg School of Medicine
                     address:
                        name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Linda J. Van Eldik
               affiliation:
                     name:Northwestern University Feinberg School of Medicine
                     address:
                        name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:MFG-E8 Regulates Microglial Phagocytosis of Apoptotic Neurons
      description:Phagocytosis is an essential mechanism for clearance of pathogens, dying cells, and other unwanted debris in order to maintain tissue health in the body. Macrophages execute this process in the peripheral immune system but in the brain microglia act as resident macrophages to accomplish this function. In the peripheral immune system, macrophages secrete Milk Fat Globule Factor-E8 (MFG-E8) that recognizes phosphatidylserine “eat me” signals expressed on the surface of apoptotic cells. MFG-E8 then acts as a tether to attach the apoptotic cell to the macrophage and trigger a signaling cascade that stimulates the phagocyte development, allowing the macrophage to engulf the dying cell. When this process becomes disrupted, inflammation and autoimmunity can result. MFG-E8 resides in the brain as well as in the periphery, and microglia express MFG-E8. However, the function of MFG-E8 in the brain has not been elucidated. We measured MFG-E8 production in the BV-2 microglial cell line and the role of this protein in the recognition and engulfment of apoptotic SY5Y neuroblastoma cells. BV-2 cells produced and released MFG-E8, which apoptotic SY5Y cells and the chemokine fractalkine further stimulated. Furthermore, MFG-E8 increased phagocytosis of apoptotic SY5Y cells, and a dominant negative form of MFG-E8 inhibited phagocytosis by BV-2 cells. Finally, brain MFG-E8 levels were altered in a mouse model of Alzheimer’s disease. Our data suggest that MFG-E8 acts in the brain via microglia to aid in clearance of apoptotic neurons, and we hypothesize that a dysregulation of this process may be involved in neurodegenerative disease.
      datePublished:2008-08-01T00:00:00Z
      dateModified:2008-08-01T00:00:00Z
      pageStart:246
      pageEnd:256
      license:https://creativecommons.org/licenses/by-nc/2.0
      sameAs:https://doi.org/10.1007/s11481-008-9118-2
      keywords:
         MFG-E8
         microglia
         phagocytosis
         apoptosis
         fractalkine
         Alzheimer’s disease
         Neurosciences
         Immunology
         Pharmacology/Toxicology
         Virology
         Cell Biology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig5_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11481-008-9118-2/MediaObjects/11481_2008_9118_Fig6_HTML.gif
      isPartOf:
         name:Journal of Neuroimmune Pharmacology
         issn:
            1557-1904
            1557-1890
         volumeNumber:3
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Abby D. Fuller
            affiliation:
                  name:Northwestern University Feinberg School of Medicine
                  address:
                     name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Linda J. Van Eldik
            affiliation:
                  name:Northwestern University Feinberg School of Medicine
                  address:
                     name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Journal of Neuroimmune Pharmacology
      issn:
         1557-1904
         1557-1890
      volumeNumber:3
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Northwestern University Feinberg School of Medicine
      address:
         name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
         type:PostalAddress
      name:Northwestern University Feinberg School of Medicine
      address:
         name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Abby D. Fuller
      affiliation:
            name:Northwestern University Feinberg School of Medicine
            address:
               name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
               type:PostalAddress
            type:Organization
      name:Linda J. Van Eldik
      affiliation:
            name:Northwestern University Feinberg School of Medicine
            address:
               name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA
      name:Department of Cell and Molecular Biology, Center for Drug Discovery and Chemical Biology, Northwestern University Feinberg School of Medicine, Chicago, USA

External Links {🔗}(197)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Particles.js
Prism.js

CDN Services {📦}

Crossref

4.64s.

LINK . SPRINGER . COM {}