Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages

Abstract: Mechanisms mediating vascular calcification recapitulate osteogenic processes encompassing bone formation and imply participation of bone related proteins such as bone morphogenetic protein-2 (BMP-2). Macrophages are amongst the cells that contribute to vascular ossification by releasing c...

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Detalles Bibliográficos
Autores principales: Dube, Prabhatchandra R., Birnbaumer, Lutz, Vazquez, Guillermo
Formato: Artículo
Lenguaje:Inglés
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/8723
Aporte de:
id I33-R139123456789-8723
record_format dspace
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic CALCIFICACION
OSTEOGENESIS
ENFERMEDADES VASCULARES
spellingShingle CALCIFICACION
OSTEOGENESIS
ENFERMEDADES VASCULARES
Dube, Prabhatchandra R.
Birnbaumer, Lutz
Vazquez, Guillermo
Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages
topic_facet CALCIFICACION
OSTEOGENESIS
ENFERMEDADES VASCULARES
description Abstract: Mechanisms mediating vascular calcification recapitulate osteogenic processes encompassing bone formation and imply participation of bone related proteins such as bone morphogenetic protein-2 (BMP-2). Macrophages are amongst the cells that contribute to vascular ossification by releasing cytokines that induce an osteogenic program in vascular smooth muscle cells, and also by becoming themselves osteoclast-like cells. In inflammatory vascular disease, the macrophage population in the vascular wall is diverse, with the M1 or inflammatory, and the M2 or anti-inflammatory macrophage types being dominant. Yet, the osteogenic potential of M1 and M2 macrophages remains unknown. Prompted by recent studies from our laboratory showing that in macrophages the Transient Receptor Potential Canonical 3 (TRPC3) channel contributes to endoplasmic reticulum (ER) stress-induced apoptosis in M1, but not in M2 macrophages, and given the strong relationship between ER stress and vascular calcification, we wished to examine whether TRPC3 would play a role in the osteogenic signaling of polarized macrophages. The findings reported here indicate that a constitutive BMP-2-dependent signaling operates in M1 macrophages, which is not affected by deletion of Trpc3 and is not subject to regulation by ER stress. Our studies suggest operation of an auto/paracrine mechanism by which BMP-2 secreted by M1 macrophages maintains constitutive activation of a BMP-2 receptor/SMAD1/5 signaling axis.
format Artículo
author Dube, Prabhatchandra R.
Birnbaumer, Lutz
Vazquez, Guillermo
author_facet Dube, Prabhatchandra R.
Birnbaumer, Lutz
Vazquez, Guillermo
author_sort Dube, Prabhatchandra R.
title Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages
title_short Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages
title_full Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages
title_fullStr Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages
title_full_unstemmed Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages
title_sort evidence for constitutive bone morphogenetic protein-2 secretion by m1 macrophages: constitutive auto/paracrine osteogenic signaling by bmp-2 in m1 macrophages
publisher Elsevier
publishDate 2019
url https://repositorio.uca.edu.ar/handle/123456789/8723
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