Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8723
Título : Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages
Autor : Dube, Prabhatchandra R. 
Birnbaumer, Lutz 
Vazquez, Guillermo 
Palabras clave : CALCIFICACIONOSTEOGENESISENFERMEDADES VASCULARES
Fecha de publicación : 2017
Editorial : Elsevier
Cita : Dube PR, Birnbaumer L, Vazquez G. Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages [en línea]. Biochemical and Biophysical Research Communications. 2017;491(1):154-158. doi:10.1016/j.bbrc.2017.07.065 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8723
Resumen : 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.
URI : https://repositorio.uca.edu.ar/handle/123456789/8723
ISSN : 0006-291X
1090-2104 (online)
Disciplina: MEDICINA
DOI: 10.1016/j.bbrc.2017.07.065
Derechos: Acceso Abierto
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