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Published in: Graefe's Archive for Clinical and Experimental Ophthalmology 10/2019

01-10-2019 | Basic Science

Lack of netrin-4 alters vascular remodeling in the retina

Authors: Sergio Crespo-Garcia, Nadine Reichhart, Jeffrey Wigdahl, Sergej Skosyrski, Norbert Kociok, Olaf Strauß, Antonia M. Joussen

Published in: Graefe's Archive for Clinical and Experimental Ophthalmology | Issue 10/2019

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Abstract

Purpose

Netrin-4 (NTN4) is a protein that plays an important role in the regulation of angiogenesis in the pathological retina. Some evidences show that it can also have a role in inflammation and vascular stability. We will explore these questions in vivo in the mature mouse retina.

Methods

We created a NTN4 knockout that expresses EGFP in mononuclear phagocytes (CSFR1-positive cells) to track inflammation in vivo in the retina by scanning laser ophthalmoscopy (SLO). Fundus angiography permitted to study blood vessels. Retinal function was assessed with electroretinography (ERG).

Results

Lack of NTN4 leads to an increased amount of amoeboid mononuclear phagocytes in the adult retina, and blood vessels displayed increased tortuosity when compared with the wildtype. Inner retina function also seemed affected in NTN4 null. Lack of NTN4 resulted in a higher persistence of hyaloid artery and spontaneous leakage in the adult retina. No differences were found regarding vessel bifurcation, vessel width, or vein/artery ratio.

Conclusions

These in vivo data show for the first time that lack of NTN4 induces changes in the retinal vascular phenotype in a non-pathological scenario. This evidence widens the role of NTN4 as a guidance cue in vascular remodeling.
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Metadata
Title
Lack of netrin-4 alters vascular remodeling in the retina
Authors
Sergio Crespo-Garcia
Nadine Reichhart
Jeffrey Wigdahl
Sergej Skosyrski
Norbert Kociok
Olaf Strauß
Antonia M. Joussen
Publication date
01-10-2019
Publisher
Springer Berlin Heidelberg
Published in
Graefe's Archive for Clinical and Experimental Ophthalmology / Issue 10/2019
Print ISSN: 0721-832X
Electronic ISSN: 1435-702X
DOI
https://doi.org/10.1007/s00417-019-04447-3

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