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

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Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1. / 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; Montanez, Eloi; Schmid, Bettina.

In: FRONT CELL DEV BIOL, Vol. 11, 06.2023, p. 1169962.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hipke, K, Pitter, B, Hruscha, A, van Bebber, F, Modic, M, Bansal, V, Lewandowski, SA, Orozco, D, Edbauer, D, Bonn, S, Haass, C, Pohl, U, Montanez, E & Schmid, B 2023, 'Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1', FRONT CELL DEV BIOL, vol. 11, pp. 1169962. https://doi.org/10.3389/fcell.2023.1169962

APA

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. (2023). Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1. FRONT CELL DEV BIOL, 11, 1169962. https://doi.org/10.3389/fcell.2023.1169962

Vancouver

Hipke K, Pitter B, Hruscha A, van Bebber F, Modic M, Bansal V et al. Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1. FRONT CELL DEV BIOL. 2023 Jun;11:1169962. https://doi.org/10.3389/fcell.2023.1169962

Bibtex

@article{6eaa8d6602af4cb88163ab1148cbd886,
title = "Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1",
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.",
author = "Katrin Hipke and Bettina Pitter and Alexander Hruscha and {van Bebber}, Frauke and Miha Modic and Vikas Bansal and Lewandowski, {Sebastian A} and Denise Orozco and Dieter Edbauer and Stefan Bonn and Christian Haass and Ulrich Pohl and Eloi Montanez and Bettina Schmid",
note = "Copyright {\textcopyright} 2023 Hipke, Pitter, Hruscha, van Bebber, Modic, Bansal, Lewandowski, Orozco, Edbauer, Bonn, Haass, Pohl, Montanez and Schmid.",
year = "2023",
month = jun,
doi = "10.3389/fcell.2023.1169962",
language = "English",
volume = "11",
pages = "1169962",
journal = "FRONT CELL DEV BIOL",
issn = "2296-634X",
publisher = "Frontiers Media S. A.",

}

RIS

TY - JOUR

T1 - Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1

AU - Hipke, Katrin

AU - Pitter, Bettina

AU - Hruscha, Alexander

AU - van Bebber, Frauke

AU - Modic, Miha

AU - Bansal, Vikas

AU - Lewandowski, Sebastian A

AU - Orozco, Denise

AU - Edbauer, Dieter

AU - Bonn, Stefan

AU - Haass, Christian

AU - Pohl, Ulrich

AU - Montanez, Eloi

AU - Schmid, Bettina

N1 - Copyright © 2023 Hipke, Pitter, Hruscha, van Bebber, Modic, Bansal, Lewandowski, Orozco, Edbauer, Bonn, Haass, Pohl, Montanez and Schmid.

PY - 2023/6

Y1 - 2023/6

N2 - 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.

AB - 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.

U2 - 10.3389/fcell.2023.1169962

DO - 10.3389/fcell.2023.1169962

M3 - SCORING: Journal article

C2 - 37384248

VL - 11

SP - 1169962

JO - FRONT CELL DEV BIOL

JF - FRONT CELL DEV BIOL

SN - 2296-634X

ER -