Lab-grown, 3D extracellular matrix particles improve cardiac function and morphology in myocardial ischemia
The promise of injection of extracellular matrix (ECM) from animal hearts as a treatment of myocardial ischemia has been limited by immune reactions and harsh ECM-damaging extraction procedures. We developed a novel method to produce lab-grown human three-dimensional (3-D) acellular ECM particles from human mesenchymal stem cells (MSCs) to mitigate product variability, immunogenicity, and preserve ECM architecture. We hypothesized that intramyocardial injection (I/M) of this novel ECM (dia ∼ 200 microns) would improve cardiac function in a postmyocardial infarction (MI) murine model. WT mice aged 8-10 wk underwent ligation of the left anterior descending coronary (LAD) artery and I/M injection of 10 μL ECM or normal saline (<i>n</i> = 10/group). Compared with control, ECM-treated hearts showed significant reduction in infarct size (<i>P</i> = 0.04), increased capillary density in ischemic myocardium (<i>P</i> = 0.01), and increased fractional shortening (FS) (<i>P</i> < 0.05) on <i>postoperative days</i> (POD) <i>14</i>, <i>21</i>, and <i>28</i> by echocardiography. There were no significant differences in immunogenic response as determined by TNFα, IL6, CD86, or CD163 levels (<i>P</i> > 0.05 for all) in the hearts. Biodistribution of fluorophore-conjugated ECM demonstrated localized epifluorescence in the heart after I/M injection, without significant peripheral end organ epifluorescence. Proteomic analysis of ischemic and perfused myocardium from control and ECM-treated hearts using LC-MS/MS (<i>n</i> = 3/group) detected significant changes in proteins involved in cardiomyocyte contractility and fatty acid metabolism. These findings suggest that 3-D ECM particles induce recovery of ischemic myocardium, by upregulating protein networks involved in cellular contractility and metabolism. Taken together, 3-D ECM particles represent a promising therapy for MI and warrant confirmatory studies in a high-fidelity large animal model.<b>NEW & NOTEWORTHY</b> Our novel lab-grown, human 3-D extracellular matrix (ECM) represents a novel therapeutic approach to prevent pathological remodeling and heart failure in an animal model of heart attack. This novel finding may help develop nonsurgical therapeutic modalities aimed at reducing the global burden of cardiovascular disease.
Authors
- Max Petersen (ORCID: https://orcid.org/0000-0003-3179-4619)
- Cynthia Xu (ORCID: https://orcid.org/0000-0002-2191-3066)
- Frank W. Sellke (ORCID: https://orcid.org/0000-0002-8886-801X)
- Mark Broadwin (ORCID: https://orcid.org/0000-0002-0393-9983)
- Dwight D. Harris (ORCID: https://orcid.org/0000-0001-8289-2740)
- M. Ruhul Abid (ORCID: https://orcid.org/0000-0003-2981-2638)
- Jeffrey A. Morgan (ORCID: https://orcid.org/0009-0006-6476-161X)
- Rayane Brinck Teixeira (ORCID: https://orcid.org/0000-0001-9749-6580)
- Christopher Stone (ORCID: https://orcid.org/0000-0001-6457-2663)
- Katerina St. Angelo
- Meghamsh Kanuparthy (ORCID: https://orcid.org/0009-0005-7581-0555)
Institutions
- John Brown University (US)
- Providence College (US)
- Brown University (US)
- Rhode Island Hospital (US)
- Xalud Therapeutics (United States) (US)
Publication Details
- Journal
- American Journal of Physiology-Heart and Circulatory Physiology
- Published
- 2024-12-20
- DOI
- https://doi.org/10.1152/ajpheart.00581.2024
- Citations
- 2
- Primary Topic
- Tissue Engineering and Regenerative Medicine
- Type
- article
- Field-Weighted Citation Impact
- 1.15
Funders
- Impact Fund
- Brown University
- Rhode Island Foundation
- National Institutes of Health
- National Heart, Lung, and Blood Institute
- National Institute of General Medical Sciences