Title | GATA factors efficiently direct cardiac fate from embryonic stem cells. |
Publication Type | Journal Article |
Year of Publication | 2013 |
Authors | Turbendian HK, Gordillo M, Tsai S-Y, Lu J, Kang G, Liu T-C, Tang A, Liu S, Fishman GI, Evans T |
Journal | Development |
Volume | 140 |
Issue | 8 |
Pagination | 1639-44 |
Date Published | 2013 Apr |
ISSN | 1477-9129 |
Keywords | Animals, Cell Differentiation, Embryonic Stem Cells, Flow Cytometry, GATA Transcription Factors, Heart, Immunohistochemistry, Mice, Morphogenesis, Myocytes, Cardiac, Patch-Clamp Techniques, Real-Time Polymerase Chain Reaction, Troponin T |
Abstract | <p>The GATA4 transcription factor is implicated in promoting cardiogenesis in combination with other factors, including TBX5, MEF2C and BAF60C. However, when expressed in embryonic stem cells (ESCs), GATA4 was shown to promote endoderm, not cardiac mesoderm. The capacity of related GATA factors to promote cardiogenesis is untested. We found that expression of the highly related gene, Gata5, very efficiently promotes cardiomyocyte fate from murine ESCs. Gata5 directs development of beating sheets of cells that express cardiac troponin T and show a full range of action potential morphologies that are responsive to pharmacological stimulation. We discovered that by removing serum from the culture conditions, GATA4 and GATA6 are each also able to efficiently promote cardiogenesis in ESC derivatives, with some distinctions. Thus, GATA factors can function in ESC derivatives upstream of other cardiac transcription factors to direct the efficient generation of cardiomyocytes.</p> |
DOI | 10.1242/dev.093260 |
Alternate Journal | Development |
PubMed ID | 23487308 |
PubMed Central ID | PMC3621482 |
Grant List | KL2 RR024997 / RR / NCRR NIH HHS / United States KL2RR024997 / RR / NCRR NIH HHS / United States HL105983 / HL / NHLBI NIH HHS / United States R01 HL111400 / HL / NHLBI NIH HHS / United States R01 HL105983 / HL / NHLBI NIH HHS / United States HL111400 / HL / NHLBI NIH HHS / United States UL1 TR000457 / TR / NCATS NIH HHS / United States |