Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

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

          Institute: MPI für molekulare Biomedizin     Collection: Jahrbuch 2016 (publ. 2015, arch)     Display Documents

ID: 717266.0, MPI für molekulare Biomedizin / Jahrbuch 2016 (publ. 2015, arch)
The Orphan Receptor Tie1 Controls Angiogenesis and Vascular Remodeling by Differentially Regulating Tie2 in Tip and Stalk Cells
Authors:Savant, S.; La Porta, S.; Budnik, A.; Busch, K.; Hu, J.; Tisch, N.; Korn, C.; Valls, A. F.; Benest, A. V.; Terhardt, D.; Qu, X.; Adams, R. H.; Baldwin, H. S.; Ruiz de Almodovar, C.; Rodewald, H. R.; Augustin, H. G.
Date of Publication (YYYY-MM-DD):2015-09-22
Title of Journal:Cell Rep
Issue / Number:11
Start Page:1761
End Page:1773
Review Status:Internal review
Audience:Not Specified
Abstract / Description:Tie1 is a mechanistically poorly characterized endothelial cell (EC)-specific orphan receptor. Yet, Tie1 deletion is embryonic lethal and Tie1 has been implicated in critical vascular pathologies, including atherosclerosis and tumor angiogenesis. Here, we show that Tie1 does not function independently but exerts context-dependent effects on the related receptor Tie2. Tie1 was identified as an EC activation marker that is expressed during angiogenesis by a subset of angiogenic tip and remodeling stalk cells and downregulated in the adult quiescent vasculature. Functionally, Tie1 expression by angiogenic EC contributes to shaping the tip cell phenotype by negatively regulating Tie2 surface presentation. In contrast, Tie1 acts in remodeling stalk cells cooperatively to sustain Tie2 signaling. Collectively, our data support an interactive model of Tie1 and Tie2 function, in which dynamically regulated Tie1 versus Tie2 expression determines the net positive or negative effect of Tie1 on Tie2 signaling.
External Publication Status:published
Document Type:Article
Communicated by:Keuker
Affiliations:MPI für molekulare Biomedizin
External Affiliations:Division of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), 69120 Heidelberg, Germany. Division of Cellular Immunology, German Cancer Research Center, 69120 Heidelberg, Germany. Biochemistry Center BZH, Heidelberg University, 69120 Heidelberg, Germany. Division of Cardiology, Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA; Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. Department of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, 48145 Munster, Germany; Faculty of Medicine, University of Munster, 48145 Munster, Germany. Division of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), 69120 Heidelberg, Germany; Department of Vascular Biology and Tumor Angiogenesis (CBTM), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany; German Cancer Consortium (DKTK), 69120 Heidelberg, Germany. Electronic address: augustin@angiogenese.de.
Identifiers:ISSN:2211-1247 (Electronic) %R 10.1016/j.celrep.2015.08... [ID No:1]
URL:http://www.ncbi.nlm.nih.gov/pubmed/26344773 [ID No:2]
The scope and number of records on eDoc is subject to the collection policies defined by each institute - see "info" button in the collection browse view.