The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages

Abstract Macrophages play pivotal roles in the progression and regression of atherosclerosis. Accumulating evidence suggests that macrophage polarization into an anti-inflammatory M2 state is a key characteristic of atherosclerotic plaques undergoing regression. However, the molecular mechanisms und...

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Autor principal:	Hwijin Kim
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/27e59185bdbe4c198bbf5e4c9cca09b4
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spelling	oai:doaj.org-article:27e59185bdbe4c198bbf5e4c9cca09b42021-12-02T16:07:49ZThe transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages10.1038/s41598-017-07381-82045-2322https://doaj.org/article/27e59185bdbe4c198bbf5e4c9cca09b42017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07381-8https://doaj.org/toc/2045-2322Abstract Macrophages play pivotal roles in the progression and regression of atherosclerosis. Accumulating evidence suggests that macrophage polarization into an anti-inflammatory M2 state is a key characteristic of atherosclerotic plaques undergoing regression. However, the molecular mechanisms underlying this potential association of the M2 polarization with atherosclerosis regression remain poorly understood. Further, human genetic factors that facilitate these anti-atherogenic processes remain largely unknown. We report that the transcription factor MafB plays pivotal roles in promoting macrophage M2 polarization. Further, MafB promotes cholesterol efflux from macrophage foam cells by directly up-regulating its key cellular mediators. Notably, MafB expression is significantly up-regulated in response to various metabolic and immunological stimuli that promote macrophage M2 polarization or cholesterol efflux, and thereby MafB mediates their beneficial effects, in both liver x receptor (LXR)-dependent and independent manners. In contrast, MafB is strongly down-regulated upon elevated pro-inflammatory signaling or by pro-inflammatory and pro-atherogenic microRNAs, miR-155 and miR-33. Using an integrative systems biology approach, we also revealed that M2 polarization and cholesterol efflux do not necessarily represent inter-dependent events, but MafB is broadly involved in both the processes. These findings highlight physiological protective roles that MafB may play against atherosclerosis progression.Hwijin KimNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hwijin Kim The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages
description	Abstract Macrophages play pivotal roles in the progression and regression of atherosclerosis. Accumulating evidence suggests that macrophage polarization into an anti-inflammatory M2 state is a key characteristic of atherosclerotic plaques undergoing regression. However, the molecular mechanisms underlying this potential association of the M2 polarization with atherosclerosis regression remain poorly understood. Further, human genetic factors that facilitate these anti-atherogenic processes remain largely unknown. We report that the transcription factor MafB plays pivotal roles in promoting macrophage M2 polarization. Further, MafB promotes cholesterol efflux from macrophage foam cells by directly up-regulating its key cellular mediators. Notably, MafB expression is significantly up-regulated in response to various metabolic and immunological stimuli that promote macrophage M2 polarization or cholesterol efflux, and thereby MafB mediates their beneficial effects, in both liver x receptor (LXR)-dependent and independent manners. In contrast, MafB is strongly down-regulated upon elevated pro-inflammatory signaling or by pro-inflammatory and pro-atherogenic microRNAs, miR-155 and miR-33. Using an integrative systems biology approach, we also revealed that M2 polarization and cholesterol efflux do not necessarily represent inter-dependent events, but MafB is broadly involved in both the processes. These findings highlight physiological protective roles that MafB may play against atherosclerosis progression.
format	article
author	Hwijin Kim
author_facet	Hwijin Kim
author_sort	Hwijin Kim
title	The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages
title_short	The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages
title_full	The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages
title_fullStr	The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages
title_full_unstemmed	The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages
title_sort	transcription factor mafb promotes anti-inflammatory m2 polarization and cholesterol efflux in macrophages
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/27e59185bdbe4c198bbf5e4c9cca09b4
work_keys_str_mv	AT hwijinkim thetranscriptionfactormafbpromotesantiinflammatorym2polarizationandcholesteroleffluxinmacrophages AT hwijinkim transcriptionfactormafbpromotesantiinflammatorym2polarizationandcholesteroleffluxinmacrophages
_version_	1718384706036170752

The transcription factor MafB promotes anti-inflammatory M2 polarization and cholesterol efflux in macrophages

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