The glucocorticoid receptor in monocyte‐derived macrophages is critical for cardiac infarct repair and remodeling
Cell‐ and tissue‐specific actions of glucocorticoids are mediated by the glucocorticoid receptor. Here, we demonstrate that the glucocorticoid receptor (GR) in macrophages is essential for cardiac healing after myocardial infarction. Compared with GRflox (wild‐type controls), GRLysMCre mice that lac...
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| creator | Galuppo, Paolo Vettorazzi, Sabine Hovelmann, Julian Scholz, Claus‐Jürgen Tuckermann, Jan Peter Bauersachs, Johann Fraccarollo, Daniela |
| description | Cell‐ and tissue‐specific actions of glucocorticoids are mediated by the glucocorticoid receptor. Here, we demonstrate that the glucocorticoid receptor (GR) in macrophages is essential for cardiac healing after myocardial infarction. Compared with GRflox (wild‐type controls), GRLysMCre mice that lacked GR in myeloid cells showed increased acute mortality as a result of cardiac rupture. Seven days after left coronary artery ligation, GRLysMCre mice exhibited worse cardiac function and adverse remodeling associated with impaired scar formation and angiogenic response to ischemic injury. Inactivation of GR altered the functional differentiation/maturation of monocyte‐derived macrophages in the infarcted myocardium. Mechanistically, CD45+/CD11b+/Ly6G−/F4/80+ macrophages isolated from GRLysMCre infarcts showed deregulation of factors that control inflammation, neovascularization, collagen degradation, and scar tissue formation. Moreover, we demonstrate that cardiac fibroblasts sorted from the ischemic myocardium of GRLysMCre mice compared with cells isolated from injured GRflox hearts displayed higher matrix metalloproteinase 2 expression, and we provide evidence that the macrophage GR regulates myofibroblast differentiation in the infarct microenvironment during the early phase of wound healing. In summary, GR signaling in macrophages, playing a crucial role in tissue‐repairing mechanisms, could be a potential therapeutic target during wound healing after ischemic myocardial injury.—Galuppo, P., Vettorazzi, S., Hövelmann, J., Scholz, C.‐J., Tuckermann, J. P., Bauersachs, J., Fraccarollo, D. The glucocorticoid receptor in monocyte‐derived macrophages is critical for cardiac infarct repair and remodeling. FASEB J. 31, 5122–5132 (2017). www.fasebj.org |
| doi_str_mv | 10.1096/fj.201700317R |
| format | Article |
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Here, we demonstrate that the glucocorticoid receptor (GR) in macrophages is essential for cardiac healing after myocardial infarction. Compared with GRflox (wild‐type controls), GRLysMCre mice that lacked GR in myeloid cells showed increased acute mortality as a result of cardiac rupture. Seven days after left coronary artery ligation, GRLysMCre mice exhibited worse cardiac function and adverse remodeling associated with impaired scar formation and angiogenic response to ischemic injury. Inactivation of GR altered the functional differentiation/maturation of monocyte‐derived macrophages in the infarcted myocardium. Mechanistically, CD45+/CD11b+/Ly6G−/F4/80+ macrophages isolated from GRLysMCre infarcts showed deregulation of factors that control inflammation, neovascularization, collagen degradation, and scar tissue formation. Moreover, we demonstrate that cardiac fibroblasts sorted from the ischemic myocardium of GRLysMCre mice compared with cells isolated from injured GRflox hearts displayed higher matrix metalloproteinase 2 expression, and we provide evidence that the macrophage GR regulates myofibroblast differentiation in the infarct microenvironment during the early phase of wound healing. In summary, GR signaling in macrophages, playing a crucial role in tissue‐repairing mechanisms, could be a potential therapeutic target during wound healing after ischemic myocardial injury.—Galuppo, P., Vettorazzi, S., Hövelmann, J., Scholz, C.‐J., Tuckermann, J. P., Bauersachs, J., Fraccarollo, D. The glucocorticoid receptor in monocyte‐derived macrophages is critical for cardiac infarct repair and remodeling. FASEB J. 31, 5122–5132 (2017). www.fasebj.org</description><identifier>ISSN: 0892-6638</identifier><identifier>EISSN: 1530-6860</identifier><identifier>DOI: 10.1096/fj.201700317R</identifier><identifier>PMID: 28768721</identifier><language>eng</language><publisher>United States: Federation of American Societies for Experimental Biology</publisher><subject>Angiogenesis ; Animals ; Antigens, Differentiation - genetics ; Antigens, Differentiation - metabolism ; CD11b antigen ; CD45 antigen ; Collagen ; Coronary artery ; Deactivation ; Deregulation ; Differentiation ; fibroblast ; Fibroblasts ; Glucocorticoids ; Heart ; Heart diseases ; Inactivation ; Injuries ; Ischemia ; Macrophages ; Macrophages - metabolism ; Macrophages - pathology ; Matrix metalloproteinase ; Metalloproteinase ; Mice ; Mice, Transgenic ; Monocytes ; Monocytes - metabolism ; Monocytes - pathology ; Myeloid cells ; Myocardial infarction ; Myocardial Infarction - genetics ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardium ; Myocardium - metabolism ; Myocardium - pathology ; Myofibroblasts - metabolism ; Myofibroblasts - pathology ; Receptors, Glucocorticoid - genetics ; Receptors, Glucocorticoid - metabolism ; Repair ; Rodents ; Signal Transduction ; Signaling ; Vascularization ; Wound healing</subject><ispartof>The FASEB journal, 2017-11, Vol.31 (11), p.5122-5132</ispartof><rights>FASEB</rights><rights>The Author(s).</rights><rights>Copyright Federation of American Societies for Experimental Biology (FASEB) Nov 2017</rights><rights>The Author(s) 2017 FASEB</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533R-7dc69fbe46875d2a36b784ec9332f27e0679b4b262a5ea7dddf385953956207d3</citedby><cites>FETCH-LOGICAL-c533R-7dc69fbe46875d2a36b784ec9332f27e0679b4b262a5ea7dddf385953956207d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1096%2Ffj.201700317R$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1096%2Ffj.201700317R$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28768721$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galuppo, Paolo</creatorcontrib><creatorcontrib>Vettorazzi, Sabine</creatorcontrib><creatorcontrib>Hovelmann, Julian</creatorcontrib><creatorcontrib>Scholz, Claus‐Jürgen</creatorcontrib><creatorcontrib>Tuckermann, Jan Peter</creatorcontrib><creatorcontrib>Bauersachs, Johann</creatorcontrib><creatorcontrib>Fraccarollo, Daniela</creatorcontrib><title>The glucocorticoid receptor in monocyte‐derived macrophages is critical for cardiac infarct repair and remodeling</title><title>The FASEB journal</title><addtitle>FASEB J</addtitle><description>Cell‐ and tissue‐specific actions of glucocorticoids are mediated by the glucocorticoid receptor. Here, we demonstrate that the glucocorticoid receptor (GR) in macrophages is essential for cardiac healing after myocardial infarction. Compared with GRflox (wild‐type controls), GRLysMCre mice that lacked GR in myeloid cells showed increased acute mortality as a result of cardiac rupture. Seven days after left coronary artery ligation, GRLysMCre mice exhibited worse cardiac function and adverse remodeling associated with impaired scar formation and angiogenic response to ischemic injury. Inactivation of GR altered the functional differentiation/maturation of monocyte‐derived macrophages in the infarcted myocardium. Mechanistically, CD45+/CD11b+/Ly6G−/F4/80+ macrophages isolated from GRLysMCre infarcts showed deregulation of factors that control inflammation, neovascularization, collagen degradation, and scar tissue formation. Moreover, we demonstrate that cardiac fibroblasts sorted from the ischemic myocardium of GRLysMCre mice compared with cells isolated from injured GRflox hearts displayed higher matrix metalloproteinase 2 expression, and we provide evidence that the macrophage GR regulates myofibroblast differentiation in the infarct microenvironment during the early phase of wound healing. In summary, GR signaling in macrophages, playing a crucial role in tissue‐repairing mechanisms, could be a potential therapeutic target during wound healing after ischemic myocardial injury.—Galuppo, P., Vettorazzi, S., Hövelmann, J., Scholz, C.‐J., Tuckermann, J. P., Bauersachs, J., Fraccarollo, D. The glucocorticoid receptor in monocyte‐derived macrophages is critical for cardiac infarct repair and remodeling. 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Here, we demonstrate that the glucocorticoid receptor (GR) in macrophages is essential for cardiac healing after myocardial infarction. Compared with GRflox (wild‐type controls), GRLysMCre mice that lacked GR in myeloid cells showed increased acute mortality as a result of cardiac rupture. Seven days after left coronary artery ligation, GRLysMCre mice exhibited worse cardiac function and adverse remodeling associated with impaired scar formation and angiogenic response to ischemic injury. Inactivation of GR altered the functional differentiation/maturation of monocyte‐derived macrophages in the infarcted myocardium. Mechanistically, CD45+/CD11b+/Ly6G−/F4/80+ macrophages isolated from GRLysMCre infarcts showed deregulation of factors that control inflammation, neovascularization, collagen degradation, and scar tissue formation. Moreover, we demonstrate that cardiac fibroblasts sorted from the ischemic myocardium of GRLysMCre mice compared with cells isolated from injured GRflox hearts displayed higher matrix metalloproteinase 2 expression, and we provide evidence that the macrophage GR regulates myofibroblast differentiation in the infarct microenvironment during the early phase of wound healing. In summary, GR signaling in macrophages, playing a crucial role in tissue‐repairing mechanisms, could be a potential therapeutic target during wound healing after ischemic myocardial injury.—Galuppo, P., Vettorazzi, S., Hövelmann, J., Scholz, C.‐J., Tuckermann, J. P., Bauersachs, J., Fraccarollo, D. The glucocorticoid receptor in monocyte‐derived macrophages is critical for cardiac infarct repair and remodeling. FASEB J. 31, 5122–5132 (2017). www.fasebj.org</abstract><cop>United States</cop><pub>Federation of American Societies for Experimental Biology</pub><pmid>28768721</pmid><doi>10.1096/fj.201700317R</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Animals Antigens, Differentiation - genetics Antigens, Differentiation - metabolism CD11b antigen CD45 antigen Collagen Coronary artery Deactivation Deregulation Differentiation fibroblast Fibroblasts Glucocorticoids Heart Heart diseases Inactivation Injuries Ischemia Macrophages Macrophages - metabolism Macrophages - pathology Matrix metalloproteinase Metalloproteinase Mice Mice, Transgenic Monocytes Monocytes - metabolism Monocytes - pathology Myeloid cells Myocardial infarction Myocardial Infarction - genetics Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardium Myocardium - metabolism Myocardium - pathology Myofibroblasts - metabolism Myofibroblasts - pathology Receptors, Glucocorticoid - genetics Receptors, Glucocorticoid - metabolism Repair Rodents Signal Transduction Signaling Vascularization Wound healing |
| title | The glucocorticoid receptor in monocyte‐derived macrophages is critical for cardiac infarct repair and remodeling |
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