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Title: Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1
Author: Hipke, Katrin
Pitter, Bettina
Hruscha, Alexander
van Bebber, Frauke
Modic, Miha
Bansal, Vikas
Lewandowski, Sebastian A.
Orozco, Denise
Edbauer, Dieter
Bonn, Stefan
Haass, Christian
Pohl, Ulrich
Montañez, Eloi
Schmid, Bettina
Keywords: Angiogènesi
Malalties neurodegeneratives
Peix zebra
Neurodegenerative Diseases
Zebra danio
Issue Date: 13-Jun-2023
Publisher: Frontiers Media
Abstract: Aggregation of the Tar DNA-binding protein of 43 kDa (TDP-43) is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia and likely contributes to disease by loss of nuclear function. Analysis of TDP-43 function in knockout zebrafish identified an endothelial directional migration and hypersprouting phenotype during development prior lethality. In human umbilical vein cells (HUVEC) the loss of TDP-43 leads to hyperbranching. We identified elevated expression of FIBRONECTIN 1 (FN1), the VASCULAR CELL ADHESION MOLECULE 1 (VCAM1), as well as their receptor INTEGRIN α4β1 (ITGA4B1) in HUVEC cells. Importantly, reducing the levels of ITGA4, FN1, and VCAM1 homologues in the TDP-43 loss-of-function zebrafish rescues the angiogenic defects indicating the conservation of human and zebrafish TDP-43 function during angiogenesis. Our study identifies a novel pathway regulated by TDP-43 important for angiogenesis during development.
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It is part of: Frontiers In Cell And Developmental Biology, 2023, vol. 11
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ISSN: 2296-634X
Appears in Collections:Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
Articles publicats en revistes (Ciències Fisiològiques)

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