A Role for Partial Endothelial-Mesenchymal Transitions in Angiogenesis?

被引:161
作者
Welch-Reardon, Katrina M. [1 ]
Wu, Nan [1 ]
Hughes, Christopher C. W. [1 ,2 ,3 ]
机构
[1] Univ Calif Irvine, Dept Mol Biol & Biochem, Irvine, CA 92697 USA
[2] Univ Calif Irvine, Dept Biomed Engn, Irvine, CA 92697 USA
[3] Univ Calif Irvine, Edwards Lifesci Ctr Adv Cardiovasc Technol, Irvine, CA 92697 USA
基金
美国国家卫生研究院;
关键词
angiogenesis; EMT; endothelial; transcription factor; GROWTH-FACTOR-BETA; TGF-BETA; CARDIAC FIBROSIS; VALVE DEVELOPMENT; KIDNEY FIBROSIS; BHLH FACTORS; E-CADHERIN; IN-VITRO; NOTCH; CELLS;
D O I
10.1161/ATVBAHA.114.303220
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The contribution of epithelial-to-mesenchymal transitions (EMT) in both developmental and pathological conditions has been widely recognized and studied. In a parallel process, governed by a similar set of signaling and transcription factors, endothelial-to-mesenchymal transitions (EndoMT) contribute to heart valve formation and the generation of cancer-associated fibroblasts. During angiogenic sprouting, endothelial cells express many of the same genes and break down basement membrane; however, they retain intercellular junctions and migrate as a connected train of cells rather than as individual cells. This has been termed a partial endothelial-to-mesenchymal transition. A key regulatory check-point determines whether cells undergo a full or a partial epithelial-to-mesenchymal transitions/endothelial-to-mesenchymal transition; however, very little is known about how this switch is controlled. Here we discuss these developmental/pathological pathways, with a particular focus on their role in vascular biology.
引用
收藏
页码:303 / 308
页数:6
相关论文
共 66 条
[1]   Experimental myocardial infarction triggers canonical Wnt signaling and endothelial-to-mesenchymal transition [J].
Aisagbonhi, Omonigho ;
Rai, Meena ;
Ryzhov, Sergey ;
Atria, Nick ;
Feoktistov, Igor ;
Hatzopoulos, Antonis K. .
DISEASE MODELS & MECHANISMS, 2011, 4 (04) :469-483
[2]   Perspectives on endothelial-to-mesenchymal transition: potential contribution to vascular remodeling in chronic pulmonary hypertension [J].
Arciniegas, Enrique ;
Frid, Maria G. ;
Douglas, Ivor S. ;
Stenmark, Kurt R. .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2007, 293 (01) :L1-L8
[3]   Heart valve development - Endothelial cell signaling and differentiation [J].
Armstrong, EJ ;
Bischoff, J .
CIRCULATION RESEARCH, 2004, 95 (05) :459-470
[4]   Analysis of the E-cadherin repressor snail in primary human cancers [J].
Becker, K.-F. ;
Rosivatz, E. ;
Blechschmidt, K. ;
Kremmer, E. ;
Sarbia, M. ;
Hoefler, H. .
CELLS TISSUES ORGANS, 2007, 185 (1-3) :204-212
[5]   Snail2 is an Essential Mediator of Twist1-Induced Epithelial Mesenchymal Transition and Metastasis [J].
Casas, Esmeralda ;
Kim, Jihoon ;
Bendesky, Andres ;
Ohno-Machado, Lucila ;
Wolfe, Cecily J. ;
Yang, Jing .
CANCER RESEARCH, 2011, 71 (01) :245-254
[6]  
Chen HF, 2014, ADVANCED CERAMICS FOR DENTISTRY, P5, DOI 10.1016/B978-0-12-394619-5.00002-X
[7]   FGF Regulates TGF-β Signaling and Endothelial-to-Mesenchymal Transition via Control of let-7 miRNA Expression [J].
Chen, Pei-Yu ;
Qin, Lingfeng ;
Barnes, Carmen ;
Charisse, Klaus ;
Yi, Tai ;
Zhang, Xinbo ;
Ali, Rahmat ;
Medina, Pedro P. ;
Yu, Jun ;
Slack, Frank J. ;
Anderson, Daniel G. ;
Kotelianski, Victor ;
Wang, Fen ;
Tellides, George ;
Simons, Michael .
CELL REPORTS, 2012, 2 (06) :1684-1696
[8]   Dkk1 and Msx2-Wnt7b Signaling Reciprocally Regulate the Endothelial-Mesenchymal Transition in Aortic Endothelial Cells [J].
Cheng, Su-Li ;
Shao, Jian-Su ;
Behrmann, Abraham ;
Krchma, Karen ;
Towler, Dwight A. .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2013, 33 (07) :1679-1689
[9]   Deadly crosstalk: Notch signaling at the intersection of EMT and cancer stem cells [J].
Espinoza, Ingrid ;
Miele, Lucio .
CANCER LETTERS, 2013, 341 (01) :41-45
[10]   Delta-Notch-and then? Protein interactions and proposed modes of repression by Hes and Hey bHLH factors [J].
Fischer, Andreas ;
Gessler, Manfred .
NUCLEIC ACIDS RESEARCH, 2007, 35 (14) :4583-4596