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      The ETS Factor, ETV2: a Master Regulator for Vascular Endothelial Cell Development

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          Abstract

          Appropriate vessel development and its coordinated function is essential for proper embryogenesis and homeostasis in the adult. Defects in vessels cause birth defects and are an important etiology of diseases such as cardiovascular disease, tumor and diabetes retinopathy. The accumulative data indicate that ETV2, an ETS transcription factor, performs a potent and indispensable function in mediating vessel development. This review discusses the recent progress of the study of ETV2 with special focus on its regulatory mechanisms and cell fate determining role in developing mouse embryos as well as somatic cells.

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          Direct conversion of fibroblasts to functional neurons by defined factors

          Thomas Vierbuchen, Austin Ostermeier, Zhiping Pang … (2010)
          Cellular differentiation and lineage commitment are considered robust and irreversible processes during development. Recent work has shown that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. This raised the question of whether transcription factors could directly induce other defined somatic cell fates, and not only an undifferentiated state. We hypothesized that combinatorial expression of neural lineage-specific transcription factors could directly convert fibroblasts into neurons. Starting from a pool of nineteen candidate genes, we identified a combination of only three factors, Ascl1, Brn2, and Myt1l, that suffice to rapidly and efficiently convert mouse embryonic and postnatal fibroblasts into functional neurons in vitro. These induced neuronal (iN) cells express multiple neuron-specific proteins, generate action potentials, and form functional synapses. Generation of iN cells from non-neural lineages could have important implications for studies of neural development, neurological disease modeling, and regenerative medicine.
          Article 0 comments Cited 903 times – based on 0 reviews     Review now
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            Molecular regulation of vessel maturation.

            Rakesh Jain (2003)
            The maturation of nascent vasculature, formed by vasculogenesis or angiogenesis, requires recruitment of mural cells, generation of an extracellular matrix and specialization of the vessel wall for structural support and regulation of vessel function. In addition, the vascular network must be organized so that all the parenchymal cells receive adequate nutrients. All of these processes are orchestrated by physical forces as well as by a constellation of ligands and receptors whose spatio-temporal patterns of expression and concentration are tightly regulated. Inappropriate levels of these physical forces or molecules produce an abnormal vasculature--a hallmark of various pathologies. Normalization of the abnormal vasculature can facilitate drug delivery to tumors and formation of a mature vasculature can help realize the promise of therapeutic angiogenesis and tissue engineering.
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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): Mol Cells
                Journal ID (iso-abbrev): Mol. Cells
                Journal ID (publisher-id): ksmcb
                Title: Molecules and Cells
                Publisher: Korean Society for Molecular and Cellular Biology
                ISSN (Print): 1016-8478
                ISSN (Electronic): 0219-1032
                Publication date (Print): 31 December 2015
                Publication date (Electronic): 21 December 2015
                Publication date PMC-release: 21 December 2015
                Volume: 38
                Issue: 12
                Pages: 1029-1036
                Affiliations
                [1 ]Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA
                [2 ]Children’s Heart Research and Outcomes Center, Emory University School of Medicine, Atlanta, GA, USA
                [3 ]Molecular and Systems Pharmacology Program, Emory University School of Medicine, Atlanta, GA, USA
                [4 ]Biochemistry, Cell Biology and Developmental Biology Program, Emory University School of Medicine, Atlanta, GA, USA
                Author notes
                [5]

                These authors contributed equally to this work.

                [* ]Correspondence: cpark23@ 123456emory.edu
                Article
                Publisher ID: molce-38-12-1029
                DOI: 10.14348/molcells.2015.0331
                PMC ID: 4696993
                PubMed ID: 26694034
                SO-VID: 6063c94c-293b-493e-a428-5053838b77f9
                Copyright © © The Korean Society for Molecular and Cellular Biology. All rights reserved.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.

                History
                Date received : 07 December 2015
                Date accepted : 10 December 2015
                Categories
                Subject: Minireview

                Keywords: cell reprogramming,endothelial cells,etv2,transcription factors
                Data availability:
                Keywords: cell reprogramming, endothelial cells, etv2, transcription factors

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