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      The emerging role of GATA transcription factors in development and disease

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          Abstract

          The GATA family of transcription factors consists of six proteins (GATA1-6) which are involved in a variety of physiological and pathological processes. GATA1/2/3 are required for differentiation of mesoderm and ectoderm-derived tissues, including the haematopoietic and central nervous system. GATA4/5/6 are implicated in development and differentiation of endoderm- and mesoderm-derived tissues such as induction of differentiation of embryonic stem cells, cardiovascular embryogenesis and guidance of epithelial cell differentiation in the adult.

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          The genomic landscapes of human breast and colorectal cancers.

          Laura Wood, D. Parsons, Siân Jones … (2007)
          Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.
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            In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytes

            Li Qian, Yu Huang, C Spencer … (2012)
            SUMMARY The reprogramming of adult cells into pluripotent cells or directly into alternative adult cell types holds great promise for regenerative medicine. We reported that cardiac fibroblasts, which represent 50% of the cells in the mammalian heart, can be directly reprogrammed to adult cardiomyocyte-like cells in vitro by the addition of Gata4, Mef2c and Tbx5 (GMT). Here, we use genetic lineage-tracing to show that resident non-myocytes in the murine heart can be reprogrammed into cardiomyocyte-like cells in vivo by local delivery of GMT after coronary ligation. Induced cardiomyocytes became bi-nucleate, assembled sarcomeres and had cardiomyocyte-like gene expression. Analysis of single cells revealed ventricular cardiomyocyte-like action potentials, beating upon electrical stimulation, and evidence of electrical coupling. In vivo delivery of GMT decreased infarct size and modestly attenuated cardiac dysfunction up to 3 months after coronary ligation. Delivery of the pro-angiogenic and fibroblast activating peptide, Thymosin β4, along with GMT, resulted in further improvements in scar area and cardiac function. These findings demonstrate that cardiac fibroblasts can be reprogrammed into cardiomyocyte-like cells in their native environment for potential regenerative purposes.
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              Heart repair by reprogramming non-myocytes with cardiac transcription factors

              Kunhua Song, Young-Jae Nam, Xiang Luo … (2012)
              The adult mammalian heart possesses little regenerative potential following injury. Fibrosis due to activation of cardiac fibroblasts impedes cardiac regeneration and contributes to loss of contractile function, pathological remodeling and susceptibility to arrhythmias. Cardiac fibroblasts account for a majority of cells in the heart and represent a potential cellular source for restoration of cardiac function following injury through phenotypic reprogramming to a myocardial cell fate. Here we show that four transcription factors, GATA4, Hand2, MEF2C and Tbx5 can cooperatively reprogram adult mouse tail-tip and cardiac fibroblasts into beating cardiac-like myocytes in vitro. Forced expression of these factors in dividing non-cardiomyocytes in mice reprograms these cells into functional cardiac-like myocytes, improves cardiac function and reduces adverse ventricular remodeling following myocardial infarction. Our results suggest a strategy for cardiac repair through reprogramming fibroblasts resident in the heart with cardiogenic transcription factors or other molecules.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Expert Rev Mol Med
                Journal ID (iso-abbrev): Expert Rev Mol Med
                Journal ID (publisher-id): ERM
                Title: Expert Reviews in Molecular Medicine
                Publisher: Cambridge University Press (Cambridge, UK )
                ISSN (Electronic): 1462-3994
                Publication date Collection: 2016
                Publication date (Electronic): 8 March 2016
                Volume: 18
                Electronic Location Identifier: e3
                Affiliations
                [1 ]Department of Pathology, GROW – School for Oncology and Developmental Biology, Maastricht University Medical Center , Maastricht, The Netherlands
                [2 ]Department of Molecular Oncology, Graduate School of Medicine and Dentistry, Tokyo Medical and Dental University , Tokyo, Japan
                Author notes
                [* ] Corresponding author:Prof Dr Manon van Engeland, Department of Pathology, GROW – School for Oncology and Developmental Biology, Maastricht University Medical Center , P.O. Box 616, 6200 MD Maastricht, The Netherlands. Tel: +31-43-3885498; Fax: +31-43-3876613; E-mail: manon.van.engeland@ 123456mumc.nl
                Article
                Publisher Item ID: S1462399416000028 Publisher ID: 00002
                DOI: 10.1017/erm.2016.2
                PMC ID: 4836206
                PubMed ID: 26953528
                SO-VID: f72f4c3b-1f7f-4730-9640-0bda079298f7
                Copyright © © Cambridge University Press 2016
                License:

                This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Page count
                Figures: 2, Tables: 3, References: 173, Pages: 15
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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