![]() ![]() At 4 days of differentiation, treatment with retinoic acid induced differentiation of the CPCs to atrial cells. The RAR agonists had a time‐of‐differentiation‐dependent effect on the HuES6‐derived CPCs. In addition, the RAR agonists were able to proliferate an independent source of CPCs, HuES6. The CPCs retained their progenitor phenotype following proliferation and the identified RAR agonists did not proliferate human cardiac fibroblasts, the major cell type in the heart. We identified retinoic acid receptor (RAR) agonists as potent proliferators of CPCs. The primary readout of this phenotypic screen was proliferation as measured by nuclear count. We have used an in vitro human induced pluripotent stem cell‐derived CPC model to screen a 10,000‐compound library containing molecules representing different target classes and compounds reported to modulate the phenotype of stem or primary cells. Identification of small molecules with the potential to selectively proliferate cardiac progenitor cells (CPCs) will aid our understanding of the signaling pathways and mechanisms involved and could ultimately provide tools for regenerative therapies for the treatment of post‐MI cardiac dysfunction. ![]()
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