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Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a brain endothelial cell line.

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Title: Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a brain endothelial cell line.
Authors: Yuki Yasutaka1 yasutaka@fukuoka-u.ac.jp, Takuya Watanabe2 twatanabe@fukuoka-u.ac.jp, Akio Nakashima1 anakashima@fukuoka-u.ac.jp, Junichi Matsumoto1 jmatsumoto@fukuoka-u.ac.jp, Koujiro Futagami1 futagami@fukuoka-u.ac.jp, Atsushi Yamauchi2 atyama@fukuoka-u.ac.jp, Yasufumi Kataoka2 ykataoka@fukuoka-u.ac.jp
Source: FEBS Letters. Jan2015, p263-268. 6p.
Subjects: Tumor necrosis factors, Amyloid beta-protein, Prions, Blood-brain barrier, Endothelial cells, Alzheimer's disease
Abstract: Disruption of beta-amyloid (Aß) transport across the blood-brain barrier is thought to cause Aß accumulation in the brain, thus leading to the development of Alzheimer's disease (AD). As AD patients show increased serum tumor necrosis factor-a (TNFa) levels, we examined the effect of TNFa on the function and expression of Aß transport-related proteins including cellular prion protein (PrPC) in the mouse brain microvascular endothelial cell line MBEC4. TNFa decreased PrPC levels and intracellular radiolabeled Aß. Similarly, anti-prion protein antibody also decreased radiolabeled Aß. These results suggest that TNFa lowers PrPC levels, which in turn, reduces Aß in the brain endothelium. [ABSTRACT FROM AUTHOR]
Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Engineering Source
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Header DbId: egs
DbLabel: Engineering Source
An: 109255126
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
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  Data: Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a brain endothelial cell line.
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  Data: <searchLink fieldCode="AR" term="%22Yuki+Yasutaka%22">Yuki Yasutaka</searchLink><relatesTo>1</relatesTo><i> yasutaka@fukuoka-u.ac.jp</i><br /><searchLink fieldCode="AR" term="%22Takuya+Watanabe%22">Takuya Watanabe</searchLink><relatesTo>2</relatesTo><i> twatanabe@fukuoka-u.ac.jp</i><br /><searchLink fieldCode="AR" term="%22Akio+Nakashima%22">Akio Nakashima</searchLink><relatesTo>1</relatesTo><i> anakashima@fukuoka-u.ac.jp</i><br /><searchLink fieldCode="AR" term="%22Junichi+Matsumoto%22">Junichi Matsumoto</searchLink><relatesTo>1</relatesTo><i> jmatsumoto@fukuoka-u.ac.jp</i><br /><searchLink fieldCode="AR" term="%22Koujiro+Futagami%22">Koujiro Futagami</searchLink><relatesTo>1</relatesTo><i> futagami@fukuoka-u.ac.jp</i><br /><searchLink fieldCode="AR" term="%22Atsushi+Yamauchi%22">Atsushi Yamauchi</searchLink><relatesTo>2</relatesTo><i> atyama@fukuoka-u.ac.jp</i><br /><searchLink fieldCode="AR" term="%22Yasufumi+Kataoka%22">Yasufumi Kataoka</searchLink><relatesTo>2</relatesTo><i> ykataoka@fukuoka-u.ac.jp</i>
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  Data: <searchLink fieldCode="JN" term="%22FEBS+Letters%22">FEBS Letters</searchLink>. Jan2015, p263-268. 6p.
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  Data: <searchLink fieldCode="DE" term="%22Tumor+necrosis+factors%22">Tumor necrosis factors</searchLink><br /><searchLink fieldCode="DE" term="%22Amyloid+beta-protein%22">Amyloid beta-protein</searchLink><br /><searchLink fieldCode="DE" term="%22Prions%22">Prions</searchLink><br /><searchLink fieldCode="DE" term="%22Blood-brain+barrier%22">Blood-brain barrier</searchLink><br /><searchLink fieldCode="DE" term="%22Endothelial+cells%22">Endothelial cells</searchLink><br /><searchLink fieldCode="DE" term="%22Alzheimer's+disease%22">Alzheimer's disease</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Disruption of beta-amyloid (Aß) transport across the blood-brain barrier is thought to cause Aß accumulation in the brain, thus leading to the development of Alzheimer's disease (AD). As AD patients show increased serum tumor necrosis factor-a (TNFa) levels, we examined the effect of TNFa on the function and expression of Aß transport-related proteins including cellular prion protein (PrPC) in the mouse brain microvascular endothelial cell line MBEC4. TNFa decreased PrPC levels and intracellular radiolabeled Aß. Similarly, anti-prion protein antibody also decreased radiolabeled Aß. These results suggest that TNFa lowers PrPC levels, which in turn, reduces Aß in the brain endothelium. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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      – Type: doi
        Value: 10.1016/j.febslet.2014.12.007
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      – Code: eng
        Text: English
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      Pagination:
        PageCount: 6
        StartPage: 263
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      – SubjectFull: Tumor necrosis factors
        Type: general
      – SubjectFull: Amyloid beta-protein
        Type: general
      – SubjectFull: Prions
        Type: general
      – SubjectFull: Blood-brain barrier
        Type: general
      – SubjectFull: Endothelial cells
        Type: general
      – SubjectFull: Alzheimer's disease
        Type: general
    Titles:
      – TitleFull: Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a brain endothelial cell line.
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            NameFull: Yuki Yasutaka
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            NameFull: Takuya Watanabe
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              M: 01
              Text: Jan2015
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