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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Yearbook 2016     Display Documents



ID: 723979.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Yearbook 2016
Notch signaling regulates venous arterialization during zebrafish fin regeneration
Authors:Kametani, Y.; Chi, N. C.; Stainier, D. Y.; Takada, S.
Date of Publication (YYYY-MM-DD):2015-05
Title of Journal:Genes Cells
Volume:20
Issue / Number:5
Start Page:427
End Page:438
Audience:Not Specified
Abstract / Description:To protect against blood pressure, a mature artery is supported by mural cells which include vascular smooth muscle cells and pericytes. To regenerate a functional vascular system, arteries should be properly reconstructed with mural cells although the mechanisms underlying artery reconstruction remain unclear. In this study, we examined the process of artery reconstruction during regeneration of the zebrafish caudal fin as a model to study arterial formation in an adult setting. During fin regeneration, the arteries and veins form a net-like vasculature called the vascular plexus, and this plexus undergoes remodeling to form a new artery and two flanking veins. We found that the new vascular plexus originates mainly from venous cells in the stump but very rarely from the arterial cells. Interestingly, these vein-derived cells contributed to the reconstructed arteries. This arterialization was dependent on Notch signaling, and further analysis showed that Notch signaling was required for the initiation of arterial gene expression. In contrast, venous remodeling did not require Notch signaling. These results provide new insights toward understanding mechanisms of vascular regeneration and illustrate the utility of the adult zebrafish fin to study this process.
Free Keywords:Animal Fins/*physiology; Animals; *Neovascularization, Physiologic; Receptors, Notch/*metabolism; *Regeneration; *Signal Transduction; Vascular Remodeling; Zebrafish/*physiology
External Publication Status:published
Document Type:Article
Communicated by:n.n.
Affiliations:MPI für physiologische und klinische Forschung
Identifiers:ISSN:1365-2443 (Electronic) 1356-9597 (Linking) %R 10.1111/gtc.12234
URL:http://www.ncbi.nlm.nih.gov/pubmed/25810153
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