Why the study?
The study investigated the merits of MRI using an elastin-binding contrast agent after myocardial infarction in mouse models with deletions of monocyte populations.
Can cardiac MRI with an elastin-specific contrast agent detect elastin deposition and differences in myocardial remodeling after myocardial infarction in mouse models with monocyte deletions?
Can cardiac MRI with an elastin-specific contrast agent detect elastin deposition and differences in myocardial remodeling after myocardial infarction in mouse models with monocyte deletions?
Cardiac MRI with an elastin-specific contrast agent can successfully detect in vivo elastin deposition and highlight differences in myocardial remodeling in mouse models of myocardial infarction.
Answers are grounded in this paper and cite their sources.
ESMA-MRI tracks post-MI elastin remodeling in CCR2-deficient mice; leaves open translation to human applications.
The aim of this study was to investigate the merits of magnetic resonance imaging (MRI) using an elastin-binding contrast agent after myocardial infarction in mouse models with deletions of monocyte populations. Permanent ligation of the left anterior descending (LAD) artery was conducted in 10 wild-type mice and 10 each of three knockout models: CX3CR-/-, CCR2-/-, and MCP-1-/-. At 7 days and 30 days after permanent ligation, cardiac MRI was performed with a 7 T-Bruker horizontal scanner for in vivo detection of elastin with an elastin/tropoelastin-specific contrast agent (ESMA). Histology was performed with staining for elastin, collagen I and III, and F4/80. Real-time PCR was conducted to quantify the expression of genes for collagen I and III, F4/80, and tumor necrosis factor alpha (TNFα). Histological and ESMA-indicated elastin areas were strongly correlated (r = 0.8). 30 days after permanent ligation, CCR2-deficient mice demonstrated higher elastin levels in the scar relative to MCP-1-/- (p < 0.04) and wild-type mice (p < 0.02). The ejection fraction was lower in CCR2-deficient mice. In vivo MRI in mouse models of MI can detect elastin deposition after myocardial infarction, highlighting the pivotal role of elastin in myocardial remodeling in mouse models with deletions of monocyte populations.
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Elkenhans et al. (2021) studied this question.
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