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  In vivo modulation of endothelial polarization by Apelin receptor signalling

Kwon, H.-B., Wang, S., Helker, C. S., Rasouli, S. J., Maischein, H.-M., Offermanns, S., et al. (2016). In vivo modulation of endothelial polarization by Apelin receptor signalling. NATURE COMMUNICATIONS, 7: 11805. doi:10.1038/ncomms11805.

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 Creators:
Kwon, Hyouk-Bum1, Author              
Wang, ShengPeng2, Author              
Helker, Christian S.M.1, Author              
Rasouli, S. Javad1, Author              
Maischein, Hans-Martin1, Author              
Offermanns, Stefan2, Author              
Herzog, Wiebke, Author
Stainier, Didier Y.R.1, Author              
Affiliations:
1Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591697              
2Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591696              

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Free keywords: FLUID SHEAR-STRESS; VASCULAR DEVELOPMENT; CARDIOVASCULAR DEVELOPMENT; MECHANOSENSORY COMPLEX; CELL POLARITY; BLOOD-FLOW; G-PROTEINS; ZEBRAFISH; ATHEROSCLEROSIS; HEARTScience & Technology - Other Topics;
 Abstract: Endothelial cells (ECs) respond to shear stress by aligning in the direction of flow. However, how ECs respond to flow in complex in vivo environments is less clear. Here we describe an endothelial-specific transgenic zebrafish line, whereby the Golgi apparatus is labelled to allow for in vivo analysis of endothelial polarization. We find that most ECs polarize within 4.5 h after the onset of vigorous blood flow and, by manipulating cardiac function, observe that flow-induced EC polarization is a dynamic and reversible process. Based on its role in EC migration, we analyse the role of Apelin signalling in EC polarization and find that it is critical for this process. Knocking down Apelin receptor function in human primary ECs also affects their polarization. Our study provides new tools to analyse the mechanisms of EC polarization in vivo and reveals an important role in this process for a signalling pathway implicated in cardiovascular disease.

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Language(s): eng - English
 Dates: 2016
 Publication Status: Published online
 Pages: 12
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: 000376972000001
DOI: 10.1038/ncomms11805
 Degree: -

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Title: NATURE COMMUNICATIONS
Source Genre: Journal
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Publ. Info: MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND : NATURE PUBLISHING GROUP
Pages: - Volume / Issue: 7 Sequence Number: 11805 Start / End Page: - Identifier: ISSN: 2041-1723