TGF-β Signaling Promotes Tissue Formation during Cardiac Valve Regeneration in Adult Zebrafish

Bensimon-Brito, Anabela; Ramkumar, Srinath; Boezio, Giulia L.M.; Guenther, Stefan; Kuenne, Carsten; Helker, Christian S.M.; Sánchez-Iranzo, Héctor; Iloska, Dijana; Piesker, Janett; Pullamsetti, Soni; Mercader, Nadia; Beis, Dimitris; Stainier, Didier Y.R. (2020). TGF-β Signaling Promotes Tissue Formation during Cardiac Valve Regeneration in Adult Zebrafish. Developmental cell, 52(1), 9-20.e7. Elsevier 10.1016/j.devcel.2019.10.027

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Cardiac valve disease can lead to severe cardiac dysfunction and is thus a frequent cause of morbidity and mortality. Its main treatment is valve replacement, which is currently greatly limited by the poor recellularization and tissue formation potential of the implanted valves. As we still lack suitable animal models to identify modulators of these processes, here we used adult zebrafish and found that, upon valve decellularization, they initiate a rapid regenerative program that leads to the formation of new functional valves. After injury, endothelial and kidney marrow-derived cells undergo cell cycle re-entry and differentiate into new extracellular matrix-secreting valve cells. The TGF-β signaling pathway promotes the regenerative process by enhancing progenitor cell proliferation as well as valve cell differentiation. These findings reveal a key role for TGF-β signaling in cardiac valve regeneration and establish the zebrafish as a model to identify and test factors promoting cardiac valve recellularization and growth.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy

UniBE Contributor:

Mercader Huber, Nadia Isabel

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISSN:

1534-5807

Publisher:

Elsevier

Language:

English

Submitter:

Nadia Isabel Mercader Huber

Date Deposited:

04 Dec 2019 16:06

Last Modified:

09 Jan 2020 01:33

Publisher DOI:

10.1016/j.devcel.2019.10.027

PubMed ID:

31786069

BORIS DOI:

10.7892/boris.135978

URI:

https://boris.unibe.ch/id/eprint/135978

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