Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.

Hardy, SA; Liesinger, L; Patrick, R; Poettler, M; Rech, L; Gindlhuber, J; Mabotuwana, NS; Ashour, D; Stangl, V; Bigland, M; Murtha, LA; Starkey, MR; Scherr, D; Hansbro, PM; Hoefler, G; Campos Ramos, G; Cochain, C; Harvey, RP; Birner-Gruenberger, R; Boyle, AJ; Rainer, PP

Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.

Hardy, SA Liesinger, L Patrick, R Poettler, M Rech, L Gindlhuber, J Mabotuwana, NS Ashour, D Stangl, V Bigland, M Murtha, LA Starkey, MR Scherr, D Hansbro, PM Hoefler, G Campos Ramos, G Cochain, C Harvey, RP Birner-Gruenberger, R Boyle, AJ Rainer, PP

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Publisher:: Elsevier
Publication Type:: Journal Article
Citation:: JACC Basic Transl Sci, 2023, 8, (12), pp. 1539-1554
Issue Date:: 2023-12

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Field	Value	Language
dc.contributor.author	Hardy, SA
dc.contributor.author	Liesinger, L
dc.contributor.author	Patrick, R
dc.contributor.author	Poettler, M
dc.contributor.author	Rech, L
dc.contributor.author	Gindlhuber, J
dc.contributor.author	Mabotuwana, NS
dc.contributor.author	Ashour, D
dc.contributor.author	Stangl, V
dc.contributor.author	Bigland, M
dc.contributor.author	Murtha, LA
dc.contributor.author	Starkey, MR
dc.contributor.author	Scherr, D
dc.contributor.author	Hansbro, PM
dc.contributor.author	Hoefler, G
dc.contributor.author	Campos Ramos, G
dc.contributor.author	Cochain, C
dc.contributor.author	Harvey, RP
dc.contributor.author	Birner-Gruenberger, R
dc.contributor.author	Boyle, AJ
dc.contributor.author	Rainer, PP
dc.date.accessioned	2024-01-25T05:28:31Z
dc.date.available	2023-05-17
dc.date.available	2024-01-25T05:28:31Z
dc.date.issued	2023-12
dc.identifier.citation	JACC Basic Transl Sci, 2023, 8, (12), pp. 1539-1554
dc.identifier.issn	2452-302X
dc.identifier.issn	2452-302X
dc.identifier.uri	http://hdl.handle.net/10453/174945
dc.description.abstract	Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascular cells in uninjured human and mouse hearts, and from M1 and M2 macrophages and myofibroblasts after MI. ECM-1 stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic and inflammatory pathways, and inhibits cardiac fibroblast migration. ECM-1 binds HuCFb cell surface receptor LRP1, and LRP1 inhibition blocks ECM-1 from stimulating fibroblast-to-myofibroblast transition, confirming a novel ECM-1-LRP1 fibrotic signaling axis. ECM-1 may represent a novel mechanism facilitating inflammation-fibrosis crosstalk.
dc.format	Electronic-eCollection
dc.language	eng
dc.publisher	Elsevier
dc.relation	http://purl.org/au-research/grants/nhmrc/GNT1079187
dc.relation	http://purl.org/au-research/grants/nhmrc/1175134
dc.relation	http://purl.org/au-research/grants/nhmrc/1074386
dc.relation.ispartof	JACC Basic Transl Sci
dc.relation.isbasedon	10.1016/j.jacbts.2023.05.010
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1102 Cardiorespiratory Medicine and Haematology, 1103 Clinical Sciences
dc.subject.classification	3201 Cardiovascular medicine and haematology
dc.title	Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.
dc.type	Journal Article
utslib.citation.volume	8
utslib.location.activity	United States
utslib.for	1102 Cardiorespiratory Medicine and Haematology
utslib.for	1103 Clinical Sciences
pubs.organisational-group	University of Technology Sydney
pubs.organisational-group	University of Technology Sydney/Faculty of Science
pubs.organisational-group	University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	University of Technology Sydney/Strength - CFI - Centre for Inflammation
utslib.copyright.status	open_access	*
dc.date.updated	2024-01-25T05:28:25Z
pubs.issue	12
pubs.publication-status	Published online
pubs.volume	8
utslib.citation.issue	12

Abstract:

Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascular cells in uninjured human and mouse hearts, and from M1 and M2 macrophages and myofibroblasts after MI. ECM-1 stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic and inflammatory pathways, and inhibits cardiac fibroblast migration. ECM-1 binds HuCFb cell surface receptor LRP1, and LRP1 inhibition blocks ECM-1 from stimulating fibroblast-to-myofibroblast transition, confirming a novel ECM-1-LRP1 fibrotic signaling axis. ECM-1 may represent a novel mechanism facilitating inflammation-fibrosis crosstalk.

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http://hdl.handle.net/10453/174945