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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/200880
Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1
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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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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. Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1. _Frontiers In Cell And Developmental Biology_. 2023. Vol. 11. [consulta: 23 de gener de 2026]. ISSN: 2296-634X. [Disponible a: https://hdl.handle.net/2445/200880]