All animal work was compliant with the Institutional Animal Care and Use Committee at North Carolina State University. The method to induce myocardial infarction in mice was based on previous studies30 (link). Briefly, male SCID Beige mice were anaesthetized with 3% isofluorane combined with 2% oxygen inhalation. Under sterile conditions, the heart was exposed by a minimally invasive left thoracotomy and acute myocardial infarction (AMI) was produced by permanent ligation of the LAD coronary artery. Immediately after AMI induction, the heart was randomized to receive one of the following four treatment arms: (1) ‘Control (PBS)’ group: intramyocardial injection of 50 μl PBS into the heart immediately after AMI; (2) ‘Control MP1’ group: intramyocardial injection of 1 × 105 Control MP1 in 50 μl PBS into the heart immediately after AMI; (3) ‘CMMP’ group: intramyocardial injection of 1 × 105 CMMPs in 50 μl PBS into the heart immediately after AMI; (4) ‘CSC’ group: intramyocardial injection of 1 × 105 CSCs in 50 μl PBS into the heart immediately after AMI. To enable visualization of Control MP1 or CMMP in a cohort of animals, we pre-labelled the Control MP1 or CMMP with Texas Red-X succinimidyl ester (1 mg ml−1 (Invitrogen, Carlsbad, California)).
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