Cargando…

Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function

Regulation of macrophage scavenger receptor (MSR) activity may be an important determinant of the extent of atherogenesis. The effect of macrophage-colony-stimulating factor (M-CSF) on this pathway was studied using a recently developed monoclonal antibody to murine MSR. M- CSF markedly and selectiv...

Descripción completa

Detalles Bibliográficos
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1994
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191609/
https://www.ncbi.nlm.nih.gov/pubmed/8046345
_version_ 1782147045066276864
collection PubMed
description Regulation of macrophage scavenger receptor (MSR) activity may be an important determinant of the extent of atherogenesis. The effect of macrophage-colony-stimulating factor (M-CSF) on this pathway was studied using a recently developed monoclonal antibody to murine MSR. M- CSF markedly and selectively increased MSR synthesis in murine macrophages: posttranslationally, the receptor appeared more stable and shifted to a predominantly surface distribution. Functionally, M-CSF enhanced modified lipoprotein uptake and increased divalent cation- independent adhesion in vitro. These results suggest a plausible mechanism whereby M-CSF production in the atheromatous plaque microenvironment could promote the recruitment and retention of mononuclear phagocytes and subsequent foam cell formation.
format Text
id pubmed-2191609
institution National Center for Biotechnology Information
language English
publishDate 1994
publisher The Rockefeller University Press
record_format MEDLINE/PubMed
spelling pubmed-21916092008-04-16 Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function J Exp Med Articles Regulation of macrophage scavenger receptor (MSR) activity may be an important determinant of the extent of atherogenesis. The effect of macrophage-colony-stimulating factor (M-CSF) on this pathway was studied using a recently developed monoclonal antibody to murine MSR. M- CSF markedly and selectively increased MSR synthesis in murine macrophages: posttranslationally, the receptor appeared more stable and shifted to a predominantly surface distribution. Functionally, M-CSF enhanced modified lipoprotein uptake and increased divalent cation- independent adhesion in vitro. These results suggest a plausible mechanism whereby M-CSF production in the atheromatous plaque microenvironment could promote the recruitment and retention of mononuclear phagocytes and subsequent foam cell formation. The Rockefeller University Press 1994-08-01 /pmc/articles/PMC2191609/ /pubmed/8046345 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function
title Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function
title_full Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function
title_fullStr Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function
title_full_unstemmed Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function
title_short Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function
title_sort macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191609/
https://www.ncbi.nlm.nih.gov/pubmed/8046345