Bone morphogenetic protein signaling promotes morphogenesis of blood vessels, wound epidermis, and actinotrichia during fin regeneration in zebrafish

Thorimbert, Valentine; König, Désirée; Marro, Jan; Ruggiero, Florence; Jaźwińska, Anna

doi:10.1096/fj.15-272955

Cited by 44 publications

(34 citation statements)

References 47 publications

(88 reference statements)

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“…The fin skeleton includes a fish-specific structure, the actinotrichia, which rely on evolutionarily conserved mechanisms to regulate their regeneration. Désirée König (Jazwinska laboratory, Fribourg University, Switzerland) showed that a complex mixture of growth factors (TGFβ, FGF, BMP) is required to regrow actinotrichia (Thorimbert et al, 2015).…”

Section: Blastema Dynamics and Tissue Remodelingmentioning

confidence: 99%

Trends in tissue repair and regeneration

et al. 2017

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The 6th EMBO conference on the Molecular and Cellular Basis of Regeneration and Tissue Repair took place in Paestum (Italy) on the 17th-21st September, 2016. The 160 scientists who attended discussed the importance of cellular and tissue plasticity, biophysical aspects of regeneration, the diverse roles of injury-induced immune responses, strategies to reactivate regeneration in mammals, links between regeneration and ageing, and the impact of non-mammalian models on regenerative medicine.

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Section: Blastema Dynamics and Tissue Remodelingmentioning

confidence: 99%

Trends in tissue repair and regeneration

et al. 2017

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“…; Thorimbert et al. ) is different to that shown by ray blastema (Yoshinari et al. ; Marí‐Beffa & Murciano, ; Whener et al.…”

Section: Discussionmentioning

confidence: 81%

“…), id1 (Thorimbert et al. ) in zebrafish or the tms β‐like gene in Xiphophorus (Offen et al. ) (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Widening control of fin inter‐rays in zebrafish and inferences about actinopterygian fins

et al. 2018

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The amputation of a teleost fin rapidly triggers an intricate maze of hierarchically regulated signalling processes which ultimately reconstruct the diverse tissues of the appendage. Whereas the generation of the fin pattern along the proximodistal axis brings with it several well-known developmental regulators, the mechanisms by which the fin widens along its dorsoventral axis remain poorly understood. Utilizing the zebrafish as an experimental model of fin regeneration and studying more than 1000 actinopterygian species, we hypothesized a connection between specific inter-ray regulatory mechanisms and the morphological variability of inter-ray membranes found in nature. To tackle these issues, both cellular and molecular approaches have been adopted and our results suggest the existence of two distinguishable inter-ray areas in the zebrafish caudal fin, a marginal and a central region. The present work associates the activity of the cell membrane potassium channel kcnk5b, the fibroblast growth factor receptor 1 and the sonic hedgehog pathway to the control of several cell functions involved in inter-ray wound healing or dorsoventral regeneration of the zebrafish caudal fin. This ray-dependent regulation controls cell migration, cell-type patterning and gene expression. The possibility that modifications of these mechanisms are responsible for phenotypic variations found in euteleostean species, is discussed.

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“…This results in the formation of an apical epidermal cap, which signals for the dedifferentiation of cells to form the distal blastema. Amputated zebrafish embryos obtained from a ptena +/− ptenb −/− in‐cross were fixed at 3 h post amputation (hpa) and subjected to in situ hybridization for detection of mmp9 transcription, which is a marker for the wound epithelium (Yoshinari, Ishida, Kudo, & Kawakami, 2009), and junbb and and1 transcription, both of which have previously been shown to be upregulated in the blastema (Thorimbert et al., 2015; Yoshinari et al., 2009). In fact, junbb expression is maintained well into the initial stage of regenerative outgrowth, indicating that junbb is a definitive distal blastema marker (Ishida, Nakajima, Kudo, & Kawakami, 2010).…”

Section: Blastema Formation Marker Suggests That the Initial Responsementioning

confidence: 99%

Impaired caudal fin‐fold regeneration in zebrafish deficient for the tumor suppressor Pten

et al. 2017

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Zebrafish are able to completely regrow their caudal fin‐folds after amputation. Following injury, wound healing occurs, followed by the formation of a blastema, which produces cells to replace the lost tissue in the final phase of regenerative outgrowth. Here we show that, surprisingly, the phosphatase and tumor suppressor Pten, an antagonist of phosphoinositide‐3‐kinase (PI3K) signaling, is required for zebrafish caudal fin‐fold regeneration. We found that homozygous knock‐out mutant (ptena−/−ptenb−/−) zebrafish embryos, lacking functional Pten, did not regenerate their caudal fin‐folds. AKT phosphorylation was enhanced, which is consistent with the function of Pten. Reexpression of Pten, but not catalytically inactive mutant Pten‐C124S, rescued regeneration, as did pharmacological inhibition of PI3K. Blastema formation, determined by in situ hybridization for the blastema marker junbb, appeared normal upon caudal fin‐fold amputation of ptena−/−ptenb−/− zebrafish embryos. Whole‐mount immunohistochemistry using specific markers indicated that proliferation was arrested in embryos lacking functional Pten, and that apoptosis was enhanced. Together, these results suggest a critical role for Pten by limiting PI3K signaling during the regenerative outgrowth phase of zebrafish caudal fin‐fold regeneration.

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Bone morphogenetic protein signaling promotes morphogenesis of blood vessels, wound epidermis, and actinotrichia during fin regeneration in zebrafish

Cited by 44 publications

References 47 publications

Trends in tissue repair and regeneration

Trends in tissue repair and regeneration

Widening control of fin inter‐rays in zebrafish and inferences about actinopterygian fins

Impaired caudal fin‐fold regeneration in zebrafish deficient for the tumor suppressor Pten

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