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Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
by
Kohlhaas, Michael
, Keidel, Linus M.
, Hristov, Michael
, Schindler, Jakob
, Maack, Christoph
, Puhl, Sarah-Lena
, Steffens, Sabine
, Hilby, Michael
, Jansen, Yvonne
in
631/250
/ 692/4017
/ 692/4019
/ 692/420
/ Animals
/ Bradycardia
/ Cannabinoid receptors
/ Cannabinoids
/ Cardiomyocytes
/ Cell size
/ Chemokines
/ Disease Models, Animal
/ Extracellular matrix
/ Heart
/ Heart attacks
/ Homeostasis
/ Humanities and Social Sciences
/ Hypertrophy
/ Inflammation
/ Inflammation - metabolism
/ Inflammation - pathology
/ Ischemia
/ Macrophages
/ Macrophages - metabolism
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Mice, Knockout
/ multidisciplinary
/ Myocardial infarction
/ Myocardial Infarction - genetics
/ Myocardial Infarction - metabolism
/ Myocardial Infarction - pathology
/ Myocardium - metabolism
/ Myocardium - pathology
/ Myocytes, Cardiac - metabolism
/ Myocytes, Cardiac - pathology
/ Phagocytes
/ Phenotypes
/ Receptors, Cannabinoid - genetics
/ Receptors, Cannabinoid - metabolism
/ Science
/ Science (multidisciplinary)
/ Ventricular Remodeling
/ Wound healing
2021
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Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
by
Kohlhaas, Michael
, Keidel, Linus M.
, Hristov, Michael
, Schindler, Jakob
, Maack, Christoph
, Puhl, Sarah-Lena
, Steffens, Sabine
, Hilby, Michael
, Jansen, Yvonne
in
631/250
/ 692/4017
/ 692/4019
/ 692/420
/ Animals
/ Bradycardia
/ Cannabinoid receptors
/ Cannabinoids
/ Cardiomyocytes
/ Cell size
/ Chemokines
/ Disease Models, Animal
/ Extracellular matrix
/ Heart
/ Heart attacks
/ Homeostasis
/ Humanities and Social Sciences
/ Hypertrophy
/ Inflammation
/ Inflammation - metabolism
/ Inflammation - pathology
/ Ischemia
/ Macrophages
/ Macrophages - metabolism
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Mice, Knockout
/ multidisciplinary
/ Myocardial infarction
/ Myocardial Infarction - genetics
/ Myocardial Infarction - metabolism
/ Myocardial Infarction - pathology
/ Myocardium - metabolism
/ Myocardium - pathology
/ Myocytes, Cardiac - metabolism
/ Myocytes, Cardiac - pathology
/ Phagocytes
/ Phenotypes
/ Receptors, Cannabinoid - genetics
/ Receptors, Cannabinoid - metabolism
/ Science
/ Science (multidisciplinary)
/ Ventricular Remodeling
/ Wound healing
2021
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Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
by
Kohlhaas, Michael
, Keidel, Linus M.
, Hristov, Michael
, Schindler, Jakob
, Maack, Christoph
, Puhl, Sarah-Lena
, Steffens, Sabine
, Hilby, Michael
, Jansen, Yvonne
in
631/250
/ 692/4017
/ 692/4019
/ 692/420
/ Animals
/ Bradycardia
/ Cannabinoid receptors
/ Cannabinoids
/ Cardiomyocytes
/ Cell size
/ Chemokines
/ Disease Models, Animal
/ Extracellular matrix
/ Heart
/ Heart attacks
/ Homeostasis
/ Humanities and Social Sciences
/ Hypertrophy
/ Inflammation
/ Inflammation - metabolism
/ Inflammation - pathology
/ Ischemia
/ Macrophages
/ Macrophages - metabolism
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Mice, Knockout
/ multidisciplinary
/ Myocardial infarction
/ Myocardial Infarction - genetics
/ Myocardial Infarction - metabolism
/ Myocardial Infarction - pathology
/ Myocardium - metabolism
/ Myocardium - pathology
/ Myocytes, Cardiac - metabolism
/ Myocytes, Cardiac - pathology
/ Phagocytes
/ Phenotypes
/ Receptors, Cannabinoid - genetics
/ Receptors, Cannabinoid - metabolism
/ Science
/ Science (multidisciplinary)
/ Ventricular Remodeling
/ Wound healing
2021
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Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
Journal Article
Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
2021
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Overview
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 692/4017
/ 692/4019
/ 692/420
/ Animals
/ Heart
/ Humanities and Social Sciences
/ Ischemia
/ Male
/ Mice
/ Myocardial Infarction - genetics
/ Myocardial Infarction - metabolism
/ Myocardial Infarction - pathology
/ Myocytes, Cardiac - metabolism
/ Myocytes, Cardiac - pathology
/ Receptors, Cannabinoid - genetics
/ Receptors, Cannabinoid - metabolism
/ Science
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