Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling

Abstract While classical cannabinoid receptors are known to crucially impact on myocardial infarction (MI) repair, a function of the cannabinoid-sensitive receptor GPR55 herein is poorly understood. We investigated the role of GPR55 in cardiac physiology and post-MI inflammation and remodelling. Glo...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Sarah-Lena Puhl, Michael Hilby, Michael Kohlhaas, Linus M. Keidel, Yvonne Jansen, Michael Hristov, Jakob Schindler, Christoph Maack, Sabine Steffens
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/6ed63596b3f548a8b8d64889955978bf
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:6ed63596b3f548a8b8d64889955978bf
record_format	dspace
spelling	oai:doaj.org-article:6ed63596b3f548a8b8d64889955978bf2021-12-02T16:08:06ZHaematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling10.1038/s41598-021-93755-y2045-2322https://doaj.org/article/6ed63596b3f548a8b8d64889955978bf2021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-93755-yhttps://doaj.org/toc/2045-2322Abstract While classical cannabinoid receptors are known to crucially impact on myocardial infarction (MI) repair, a function of the cannabinoid-sensitive receptor GPR55 herein is poorly understood. We investigated the role of GPR55 in cardiac physiology and post-MI inflammation and remodelling. Global GPR55−/− and wildtype (WT) mice were basally characterized or assigned to 1, 3 or 28 days permanent MI and subsequently analysed via pro-inflammatory and pro-hypertrophic parameters. GPR55−/− deficiency was basally associated with bradycardia, increased diastolic LV volume and sarcomere length and a subtle inflammatory phenotype. While infarct size and myeloid cell infiltration were unaffected by GPR55 depletion, acute cardiac chemokine production was prolonged post-MI. Concurrently, GPR55−/− hearts exhibited a premature expansion of pro-reparative and phagocytic macrophages paralleled by early up-regulation of extracellular matrix (ECM) factors 3 days post-MI, which could be mimicked by sole haematopoietic GPR55 depletion. Moreover, global GPR55 deficiency mitigated MI-induced foetal gene re-programming and cardiomyocyte hypertrophy, culminating in aggravated LV dilatation and infarct expansion. GPR55 regulates cardiac homeostasis and ischaemia responses by maintaining adequate LV filling and modulating three crucial processes post-MI: wound healing kinetics, cardiomyocyte hypertrophy and maladaptive remodelling.Sarah-Lena PuhlMichael HilbyMichael KohlhaasLinus M. KeidelYvonne JansenMichael HristovJakob SchindlerChristoph MaackSabine SteffensNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sarah-Lena Puhl Michael Hilby Michael Kohlhaas Linus M. Keidel Yvonne Jansen Michael Hristov Jakob Schindler Christoph Maack Sabine Steffens Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
description	Abstract While classical cannabinoid receptors are known to crucially impact on myocardial infarction (MI) repair, a function of the cannabinoid-sensitive receptor GPR55 herein is poorly understood. We investigated the role of GPR55 in cardiac physiology and post-MI inflammation and remodelling. Global GPR55−/− and wildtype (WT) mice were basally characterized or assigned to 1, 3 or 28 days permanent MI and subsequently analysed via pro-inflammatory and pro-hypertrophic parameters. GPR55−/− deficiency was basally associated with bradycardia, increased diastolic LV volume and sarcomere length and a subtle inflammatory phenotype. While infarct size and myeloid cell infiltration were unaffected by GPR55 depletion, acute cardiac chemokine production was prolonged post-MI. Concurrently, GPR55−/− hearts exhibited a premature expansion of pro-reparative and phagocytic macrophages paralleled by early up-regulation of extracellular matrix (ECM) factors 3 days post-MI, which could be mimicked by sole haematopoietic GPR55 depletion. Moreover, global GPR55 deficiency mitigated MI-induced foetal gene re-programming and cardiomyocyte hypertrophy, culminating in aggravated LV dilatation and infarct expansion. GPR55 regulates cardiac homeostasis and ischaemia responses by maintaining adequate LV filling and modulating three crucial processes post-MI: wound healing kinetics, cardiomyocyte hypertrophy and maladaptive remodelling.
format	article
author	Sarah-Lena Puhl Michael Hilby Michael Kohlhaas Linus M. Keidel Yvonne Jansen Michael Hristov Jakob Schindler Christoph Maack Sabine Steffens
author_facet	Sarah-Lena Puhl Michael Hilby Michael Kohlhaas Linus M. Keidel Yvonne Jansen Michael Hristov Jakob Schindler Christoph Maack Sabine Steffens
author_sort	Sarah-Lena Puhl
title	Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
title_short	Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
title_full	Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
title_fullStr	Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
title_full_unstemmed	Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
title_sort	haematopoietic and cardiac gpr55 synchronize post-myocardial infarction remodelling
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/6ed63596b3f548a8b8d64889955978bf
work_keys_str_mv	AT sarahlenapuhl haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT michaelhilby haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT michaelkohlhaas haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT linusmkeidel haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT yvonnejansen haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT michaelhristov haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT jakobschindler haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT christophmaack haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling AT sabinesteffens haematopoieticandcardiacgpr55synchronizepostmyocardialinfarctionremodelling
_version_	1718384602991558656

Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling

Ejemplares similares