Factors produced by activated macrophages reduce accumulation of Alzheimer's β-amyloid protein in vascular smooth muscle cells

Bozena Mazur-Kolecka; Janusz Frackowiak; Harry Le Vine; Taraneh Haske; Henryk M. Wisniewski

doi:10.1016/S0006-8993(97)00327-2

Factors produced by activated macrophages reduce accumulation of Alzheimer's β-amyloid protein in vascular smooth muscle cells

Bozena Mazur-Kolecka, Janusz Frackowiak, Harry Le Vine, Taraneh Haske, Henryk M. Wisniewski

Molecular and Cellular Biochemistry

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

Abstract

Smooth muscle cells (SMCs) isolated from amyloid-angiopathy affected brain vessels accumulate intracellularly amyloid-β peptide (Aβ). Now we demonstrate that accumulation of Aβ in SMCs can be reduced by factors secreted by macrophages - IL-1 α, IL-6, TNF-α, TGF-β1 or PGE₂- probably by stimulating the non-amyloidogenic processing of A β precursor protein (PP). It is suggested that brain macrophages may regulate AβPP/A β metabolism under physiological conditions and prevent β-amyloidosis. The disturbance of this regulatory function of brain macrophages may result in excessive production and accumulation of A β.

Original language	English
Pages (from-to)	255-260
Number of pages	6
Journal	Brain Research
Volume	760
Issue number	1-2
DOIs	https://doi.org/10.1016/S0006-8993(97)00327-2
State	Published - Jun 20 1997

Bibliographical note

Funding Information:
The authors thank Dr. K.S. Kim for mAb 4G8 and 6E10, Dr. P. Mehta for antiserum R-57, and T. Sukontasup (all from for IBR, Staten Island, NY) for skillful technical assistance. Supported in part by funds from the New York State Office of Mental Retardation and Developmental Disabilities and grants from the National Institute of Aging, NIH, Nos. 1 R03 AG14165-01 and PO1 AG 04220.

Funding

The authors thank Dr. K.S. Kim for mAb 4G8 and 6E10, Dr. P. Mehta for antiserum R-57, and T. Sukontasup (all from for IBR, Staten Island, NY) for skillful technical assistance. Supported in part by funds from the New York State Office of Mental Retardation and Developmental Disabilities and grants from the National Institute of Aging, NIH, Nos. 1 R03 AG14165-01 and PO1 AG 04220.

Funders	Funder number
New York State Office of Mental Retardation and Developmental Disabilities
National Institutes of Health (NIH)	1 R03 AG14165-01
National Institute on Aging	P01AG004220

Keywords

Amyloid-β accumulation
Amyloid-β precursor protein processing
Monokines
Smooth muscle cell

ASJC Scopus subject areas

General Neuroscience
Molecular Biology
Clinical Neurology
Developmental Biology

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10.1016/S0006-8993(97)00327-2

Cite this

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title = "Factors produced by activated macrophages reduce accumulation of Alzheimer's β-amyloid protein in vascular smooth muscle cells",

abstract = "Smooth muscle cells (SMCs) isolated from amyloid-angiopathy affected brain vessels accumulate intracellularly amyloid-β peptide (Aβ). Now we demonstrate that accumulation of Aβ in SMCs can be reduced by factors secreted by macrophages - IL-1 α, IL-6, TNF-α, TGF-β1 or PGE2- probably by stimulating the non-amyloidogenic processing of A β precursor protein (PP). It is suggested that brain macrophages may regulate AβPP/A β metabolism under physiological conditions and prevent β-amyloidosis. The disturbance of this regulatory function of brain macrophages may result in excessive production and accumulation of A β.",

keywords = "Amyloid-β accumulation, Amyloid-β precursor protein processing, Monokines, Smooth muscle cell",

author = "Bozena Mazur-Kolecka and Janusz Frackowiak and {Le Vine}, Harry and Taraneh Haske and Wisniewski, {Henryk M.}",

note = "Funding Information: The authors thank Dr. K.S. Kim for mAb 4G8 and 6E10, Dr. P. Mehta for antiserum R-57, and T. Sukontasup (all from for IBR, Staten Island, NY) for skillful technical assistance. Supported in part by funds from the New York State Office of Mental Retardation and Developmental Disabilities and grants from the National Institute of Aging, NIH, Nos. 1 R03 AG14165-01 and PO1 AG 04220.",

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doi = "10.1016/S0006-8993(97)00327-2",

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AU - Mazur-Kolecka, Bozena

AU - Frackowiak, Janusz

AU - Le Vine, Harry

AU - Haske, Taraneh

AU - Wisniewski, Henryk M.

N1 - Funding Information: The authors thank Dr. K.S. Kim for mAb 4G8 and 6E10, Dr. P. Mehta for antiserum R-57, and T. Sukontasup (all from for IBR, Staten Island, NY) for skillful technical assistance. Supported in part by funds from the New York State Office of Mental Retardation and Developmental Disabilities and grants from the National Institute of Aging, NIH, Nos. 1 R03 AG14165-01 and PO1 AG 04220.

PY - 1997/6/20

Y1 - 1997/6/20

N2 - Smooth muscle cells (SMCs) isolated from amyloid-angiopathy affected brain vessels accumulate intracellularly amyloid-β peptide (Aβ). Now we demonstrate that accumulation of Aβ in SMCs can be reduced by factors secreted by macrophages - IL-1 α, IL-6, TNF-α, TGF-β1 or PGE2- probably by stimulating the non-amyloidogenic processing of A β precursor protein (PP). It is suggested that brain macrophages may regulate AβPP/A β metabolism under physiological conditions and prevent β-amyloidosis. The disturbance of this regulatory function of brain macrophages may result in excessive production and accumulation of A β.

AB - Smooth muscle cells (SMCs) isolated from amyloid-angiopathy affected brain vessels accumulate intracellularly amyloid-β peptide (Aβ). Now we demonstrate that accumulation of Aβ in SMCs can be reduced by factors secreted by macrophages - IL-1 α, IL-6, TNF-α, TGF-β1 or PGE2- probably by stimulating the non-amyloidogenic processing of A β precursor protein (PP). It is suggested that brain macrophages may regulate AβPP/A β metabolism under physiological conditions and prevent β-amyloidosis. The disturbance of this regulatory function of brain macrophages may result in excessive production and accumulation of A β.

KW - Amyloid-β accumulation

KW - Amyloid-β precursor protein processing

KW - Monokines

KW - Smooth muscle cell

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Factors produced by activated macrophages reduce accumulation of Alzheimer's β-amyloid protein in vascular smooth muscle cells

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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