Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

Quick Search
My eDoc
Support Wiki
Direct access to
document ID:

          Document History for Document ID 744098

Back to latest document version
Document Version Version Comment Date Status
744098.0 [No comment] 19.12.2018 14:41 Released

ID: 744098.0, MPI für molekulare Biomedizin / Jahrbuch 2018 (publ. 2017, arch)
Endoglin controls blood vessel diameter through endothelial cell shape changes in response to haemodynamic cues
Authors:Sugden, W. W.; Meissner, R.; Aegerter-Wilmsen, T.; Tsaryk, R.; Leonard, E. V.; Bussmann, J.; Hamm, M. J.; Herzog, W.; Jin, Y.; Jakobsson, L.; Denz, C.; Siekmann, A. F.
Date of Publication (YYYY-MM-DD):2017-06
Title of Journal:Nat Cell Biol
Issue / Number:6
Start Page:653
End Page:665
Review Status:Internal review
Audience:Not Specified
Abstract / Description:The hierarchical organization of properly sized blood vessels ensures the correct distribution of blood to all organs of the body, and is controlled via haemodynamic cues. In current concepts, an endothelium-dependent shear stress set point causes blood vessel enlargement in response to higher flow rates, while lower flow would lead to blood vessel narrowing, thereby establishing homeostasis. We show that during zebrafish embryonic development increases in flow, after an initial expansion of blood vessel diameters, eventually lead to vessel contraction. This is mediated via endothelial cell shape changes. We identify the transforming growth factor beta co-receptor endoglin as an important player in this process. Endoglin mutant cells and blood vessels continue to enlarge in response to flow increases, thus exacerbating pre-existing embryonic arterial-venous shunts. Together, our data suggest that cell shape changes in response to biophysical cues act as an underlying principle allowing for the ordered patterning of tubular organs.
Free Keywords:Animals; Arteriovenous Malformations/genetics/metabolism/physiopathology; *Cell Shape; Endoglin/deficiency/genetics/*metabolism; Endothelial Cells/*metabolism; Genetic Predisposition to Disease; *Hemodynamics; Human Umbilical Vein Endothelial Cells/metabolism; Humans; Kruppel-Like Transcription Factors/genetics/metabolism; *Mechanotransduction, Cellular; Mice, Knockout; Mutation; Neovascularization, Physiologic; Phenotype; Regional Blood Flow; Stress, Mechanical; Time Factors; Zebrafish/embryology/genetics/metabolism; Zebrafish Proteins/genetics/*metabolism
External Publication Status:published
Document Type:Article
Communicated by:MPI für molekulare Biomedizin
Affiliations:MPI für molekulare Biomedizin
External Affiliations:Cells-in-Motion Cluster of Excellence (EXC 1003 - CiM), University of Muenster, D-48149 Muenster, Germany. Institute of Applied Physics and Center for Nonlinear Science (CeNoS), University of Muenster, D-48149 Muenster, Germany. Institute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland. University of Muenster, D-48149 Muenster, Germany. Karolinska Institute, Department of Medical Biochemistry and Biophysics, SE 171 77 Stockholm, Sweden.
Identifiers:ISSN:1476-4679 (Electronic) 1465-7392 (Linking) %R 10.1... [ID No:1]
URL:https://www.ncbi.nlm.nih.gov/pubmed/28530658 [ID No:2]