dc.contributor.author
Kociok, Norbert
dc.contributor.author
Crespo-Garcia, Sergio
dc.contributor.author
Liang, Yong
dc.contributor.author
Klein, Sabrina V.
dc.contributor.author
Nürnberg, Christina
dc.contributor.author
Reichhart, Nadine
dc.contributor.author
Skosyrski, Sergej
dc.contributor.author
Moritz, Eva
dc.contributor.author
Maier, Anna-Karina
dc.contributor.author
Brunken, William J.
dc.contributor.author
Strauß, Olaf
dc.contributor.author
Koch, Manuel
dc.contributor.author
Joussen, Antonia M.
dc.date.accessioned
2018-06-08T03:04:37Z
dc.date.available
2016-02-22T12:19:30.910Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/14463
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-18655
dc.description.abstract
Netrins are a family of matrix-binding proteins that function as guidance
signals. Netrin-4 displays pathologic roles in tumorigenesis and
neovascularization. To answer the question whether netrin-4 acts either pro-
or anti-angiogenic, angiogenesis in the retina was assessed in Ntn-4−/− mice
with oxygen-induced retinopathy (OIR) and laser-induced choroidal
neovascularization (CNV), mimicking hypoxia-mediated neovascularization and
inflammatory mediated angiogenesis. The basement membrane protein netrin-4 was
found to be localised to mature retinal blood vessels. Netrin-4, but not
netrin-1 mRNA expression, increased in response to relative hypoxia and
recovered to normal levels at the end of blood vessel formation. No changes in
the retina were found in normoxic Ntn-4−/− mice. In OIR, Ntn-4−/− mice
initially displayed larger avascular areas which recovered faster to
revascularization. Ganzfeld electroretinography showed faster recovery of
retinal function in Ntn-4−/− mice. Expression of netrin receptors, Unc5H2
(Unc-5 homolog B, C. elegans) and DCC (deleted in colorectal carcinoma), was
found in Müller cells and astrocytes. Laser-induced neovascularization in
Nnt-4−/− mice did not differ to that in the controls. Our results indicate a
role for netrin-4 as an angiogenesis modulating factor in O2-dependent
vascular homeostasis while being less important during normal retinal
developmental angiogenesis or during inflammatory neovascularization.
en
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.title
Lack of netrin-4 modulates pathologic neovascularization in the eye
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
Scientific Reports. - 6 (2016), Artikel Nr. 18828
dcterms.bibliographicCitation.doi
10.1038/srep18828
dcterms.bibliographicCitation.url
http://www.nature.com/articles/srep18828
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000023937
refubium.note.author
Der Artikel wurde in einer reinen Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000006017
dcterms.accessRights.openaire
open access