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Mechanosensitive β-catenin signaling regulates lymphatic vascular development
Mechanosensitive β-catenin signaling regulates lymphatic vascular development
BMB Reports. 2016. Aug, 49(8): 403-404
Copyright © 2016, Korean Society for Biochemistry and Molecular Biology
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • Received : July 14, 2016
  • Published : August 31, 2016
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About the Authors
Boksik, Cha
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation
R. Sathish, Srinivasan
Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA
Sathish-Srinivasan@omrf.org

Abstract
The Wnt/β-catenin signaling is an evolutionarily conserved pathway that plays a pivotal role in embryonic development and adult homeostasis. However, we have limited information about the involvement of Wnt/β-catenin signaling in the lymphatic vascular system that regulates fluid homeostasis by absorbing interstitial fluid and returning it to blood circulation. In this recent publication we report that canonical Wnt/β-catenin signaling is highly active and critical for the formation of lymphovenus valves (LVVs) and lymphatic valves (LVs). β-catenin directly associates with the regulatory elements of the lymphedema-associated transcription factor, FOXC2 and activates its expression in an oscillatory shear stress (OSS)-dependent manner. The phenotype of β-catenin null embryos was rescued by FOXC2 overexpression. These results suggest that Wnt/β-catenin signaling is a mechanotransducer that links fluid force with lymphatic vascular development. [BMB Reports 2016; 49(8): 403-404]
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Acknowledgements
RSS is supported by NIH/NHLBI (R01HL131652), institutional funds of OMRF, Oklahoma Center for Adult Stem Cell Research (OCASCR, 4340) and American Heart Association (15BGIA25710032). BC is supported by a post-doctoral fellowship from American Heart Association (15POST25080182).
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