Research Interest

My Ph.D. studies in embryology conducted me to the analysis of the function of tyrosine hydroxylase (TH), the limiting enzyme in the biosynthesis pathway of catecholamines, during heart development. The obtained results showed that TH is present in cells committed to form the heart at stages where no traces of neuron development are detected. Moreover, this enzyme seems to play a role during heart chamber formation in chicken embryos. Catecholamines’ precursor, L-DOPA, and dopamine improved cardiac differentiation/maturation in several mouse embryonic stem cell (mESC) lines. During the time I was analyzing TH function in early stages of cardiogenesis, a population of cardiac progenitor cells was described, marked by the LIM-homeodomain-containing transcription factor ISL1. ISL1 cardiac progenitor cells (ICPCs) are present in the second or anterior heart field (SHF/AHF) and give rise to the 3 main lineages in the heart: cardiomyocytes, smooth muscle cells and endothelial cells. The differentiation potential of ICPCs together with their proliferative capacity, make them a valuable cell source to be considered in cell therapies to treat cardiovascular diseases.

In 2011, I joined Dr. Qyang’s lab at Yale Cardiovascular Research Center. In collaboration with surgeons from the Department, I started to study the potential of mouse ICPCs in heart regeneration after myocardial infarction. These studies demonstrated that ICPCs survive in infarcted hearts and differentiate in vivo to cardiomyocytes and endothelial cells. These endothelial cells can integrate in host blood vessels. Additionally, implanted ICPCs alleviated the disease as shown by fractional shortening and ejection fraction measurements.

Currently I am studying human ICPCs to analyze their in vitro differentiation potential and the factors involved in the specific differentiation to cardiomyocytes, smooth muscle cells or endothelial cells. Once human ICPCs committed to form working myocardium are identified, my purpose is the application of these cells in mammal models of myocardium infarction.