PUBLICATION

Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1

Authors
Hipke, K., Pitter, B., Hruscha, A., van Bebber, F., Modic, M., Bansal, V., Lewandowski, S.A., Orozco, D., Edbauer, D., Bonn, S., Haass, C., Pohl, U., Montanez, E., Schmid, B.
ID
ZDB-PUB-230630-27
Date
2023
Source
Frontiers in cell and developmental biology   11: 11699621169962 (Journal)
Registered Authors
Haass, Christian, Hruscha, Alexander, Schmid, Bettina, van Bebber, Frauke
Keywords
ALS, TDP-43, angiogenesis, neurodegeneration, zebrafish
MeSH Terms
none
PubMed
37384248 Full text @ Front Cell Dev Biol
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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Sequence Targeting Reagents
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