Article ; Online: GDF5 deficiency prevents cardiac rupture following acute myocardial infarction in mice.
Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
2023 Volume 68, Page(s) 107581
Abstract: Background: We previously showed that growth differentiation factor 5 (GDF5) limits infarct expansion post-myocardial infarction (MI). We now examine the acute post-MI role of GDF5 in cardiac rupture.: Methods and results: Following permanent ... ...
Abstract | Background: We previously showed that growth differentiation factor 5 (GDF5) limits infarct expansion post-myocardial infarction (MI). We now examine the acute post-MI role of GDF5 in cardiac rupture. Methods and results: Following permanent ligation of the left anterior descending artery, GDF5 deficiency (i.e., GDF5 knockout mice) reduced the incidence of cardiac rupture (4/24 vs. 17/24; P < .05), and improved survival over 28-d compared to wild-type (WT) mice (79% vs. 25%; P < .0001). Moreover, at 3-d post-MI, GDF5-deficient mice manifest: (a) reduced heart weight/body weight ratio (P < .0001) without differences in infarct size or cardiomyocyte size; (b) increased infarct zone expression of Col1a1 (P < .05) and Col3a1 (P < .01), suggesting increased myocardial fibrosis; and (c) reduced aortic and left ventricular peak systolic pressures (P ≤ .05), suggesting reduced afterload. Despite dysregulated inflammatory markers and reduced circulating monocytes in GDF5-deficient mice at 3-d post-MI, reciprocal bone marrow transplantation (BMT) failed to implicate GDF5 in BM-derived cells, suggesting the involvement of tissue-resident GDF5 expression in cardiac rupture. Conclusions: Loss of GDF5 reduces cardiac rupture post-MI with increased myocardial fibrosis and lower afterload, albeit at the cost of chronic adverse remodeling. |
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MeSH term(s) | Animals ; Mice ; Disease Models, Animal ; Fibrosis ; Growth Differentiation Factor 5/genetics ; Growth Differentiation Factor 5/metabolism ; Heart Rupture/genetics ; Heart Rupture/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial Infarction/complications ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; Myocardium/pathology |
Chemical Substances | Growth Differentiation Factor 5 |
Language | English |
Publishing date | 2023-10-13 |
Publishing country | United States |
Document type | Journal Article |
ZDB-ID | 1134600-0 |
ISSN | 1879-1336 ; 1054-8807 |
ISSN (online) | 1879-1336 |
ISSN | 1054-8807 |
DOI | 10.1016/j.carpath.2023.107581 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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