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Characterization of Cardiac Progenitor Cells from Adult Murine Skeletal Muscle
Author(s) -
Pacak Christina A,
Alpatov Ivan,
Fullen Shelby,
Emmer Sawyer F,
Cowan Douglas B
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1146.5
Subject(s) - microbiology and biotechnology , embryonic stem cell , progenitor cell , population , skeletal muscle , biology , transgene , cardiac muscle , regenerative medicine , genetically modified mouse , myocyte , stem cell , chemistry , anatomy , gene , genetics , medicine , environmental health
We have identified a cell population from the hind‐limb muscles of adult mice that possesses the potential to yield therapeutically‐relevant quantities of autologous cells for cardiac regenerative therapies. Using transgenic knock‐in mice, cells expressing the evolutionarily‐conserved transcription factors Islet‐1 and Nkx2–5, which direct cardiac specification during embryonic development, were selectively marked in post‐natal tissues. These non‐adherent, muscle‐derived cardiac progenitor (MDCP) cells spontaneously beat in culture, show a rapid growth potential, and express proteins essential in regulating cardiac lineage commitment. MDCPs were expanded in orbital bioreactors and characterized by a variety of gene expression, morphological and electrophysiological analyses. Our protocol yields cells that increasingly express cardiac‐specific genes over time. When attached to multi‐electrode arrays, MDCPs display action potential amplitudes resembling those of cardiomyocytes. Co‐culture experiments show electrical synchronization of MDCPs with neonatal cardiomyocytes and elongation of MDCP action potential duration along with slowing of conduction velocity. In conclusion, we are developing techniques to isolate, proliferate, and differentiate a population of cardiac progenitors in order to advance cell‐based therapies for the heart. Support ‐ NIH HL088206 and AHA 11910008.