Kragl, M.* ; Schubert, R.* ; Karsjens, H.* ; Otter, S.* ; Bartosinska, B.* ; Jeruschke, K.* ; Weiss, J.* ; Chen, C. ; Alsteens, D.* ; Kuss, O.* ; Speier, S. ; Eberhard, D.* ; Müller, D.J.* ; Lammert, E.*
The biomechanical properties of an epithelial tissue determine the location of its vasculature.
Nat. Commun. 7:13560 (2016)
An important question is how growing tissues establish a blood vessel network. Here we study vascular network formation in pancreatic islets, endocrine tissues derived from pancreatic epithelium. We find that depletion of integrin-linked kinase (ILK) in the pancreatic epithelial cells of mice results in glucose intolerance due to a loss of the intra-islet vasculature. In turn, blood vessels accumulate at the islet periphery. Neither alterations in endothelial cell proliferation, apoptosis, morphology, Vegfa expression and VEGF-A secretion nor empty sleeves' of vascular basement membrane are found. Instead, biophysical experiments reveal that the biomechanical properties of pancreatic islet cells, such as their actomyosin-mediated cortex tension and adhesive forces to endothelial cells, are significantly changed. These results suggest that a sorting event is driving the segregation of endothelial and epithelial cells and indicate that the epithelial biomechanical properties determine whether the blood vasculature invades or envelops a growing epithelial tissue.
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Publication type
Article: Journal article
Document type
Scientific Article
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Editors
Keywords
Integrin-linked Kinase; Endothelial Growth-factor; Beta-cell Mass; Cortical Tension; Tumor Angiogenesis; Intercellular-adhesion; Differential Adhesion; Force Spectroscopy; Insulin-secretion; Blood-vessels
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Language
english
Publication Year
2016
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2016
ISSN (print) / ISBN
2041-1723
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2041-1723
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Article Number: 13560
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Nature Publishing Group
Publishing Place
London
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Peer reviewed
Institute(s)
Institute of Pancreatic Islet Research (IPI)
POF-Topic(s)
90000 - German Center for Diabetes Research
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-502600-005
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Erfassungsdatum
2016-12-31