Keeping your vascular integrity: What can we learn from fish?

Luttun, Aernout; Verhamme, Peter

doi:10.1002/bies.20755

Cited by 7 publications

(5 citation statements)

References 40 publications

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“…Activation of caspases is a key event for the induction of apoptosis, but antiapoptotic proteins of the IAPs family block the caspase-induced apoptosis (37,38). Among antiapoptotic proteins, cellular BIRC2 and BIRC3 have been identified as components of a plasma membrane-bound signaling complex I containing themselves, tumor necrosis factor receptor (TNFR), RIP1, TNFR-associated factor 2 (TRAF2) and the TNFRassociated death domain (TRADD) to confer prosurvival properties (39,40). BIRC2 and BIRC3 are found to regulate prosurvival NF-kB pathway in the non-canonical pathway by ubiquitination of NF-kBinducing kinase (NIK) and in the canonical pathway by ubiquitinating RIP1 and enabling recruitment of IKK kinase and E3 ubiquitin ligase complex LUBAC (41)(42)(43).…”

Section: Discussionmentioning

confidence: 99%

The Zebrafish Antiapoptotic Protein BIRC2 Promotes Edwardsiella piscicida Infection by Inhibiting Caspases and Accumulating p53 in a p53 Transcription-Dependent and -Independent Manner

et al. 2021

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IAPs (inhibitors of apoptosis) are endogenous caspase inhibitors with multiple biological activities. In the present study, we show functional characteristics of antiapoptotic protein BIRC2 (cIAP1) in response to Edwardsiella piscicida infection. Overexpression of BIRC2 in zebrafish larvae promoted the proliferation of E. piscicida, leading to a decreased larvae survival. The expression levels of caspases including casp3, casp8, and casp9 were significantly inhibited by BIRC2 overexpression in the case of E. piscicida infection. Treatment of zebrafish larvae microinjected with BIRC2 with the caspase activator PAC-1 completely blocked the negative regulation of BIRC2 on the E. piscicida infection, with the reduced inhibition on the casp3 and without inhibition on casp8 and casp9. In contrast to the regulation of BIRC2 on the caspases, BIRC2 overexpression significantly induced the expression of p53, especially at 24 hpi. In addition to the cytoplasmic p53 expression, BIRC2 overexpression also induced the expression of the nuclear p53 protein. Further analysis demonstrated that BIRC2 could interact and colocalize with p53 in the cytoplasm. The numbers of E. piscicida in larvae overexpressed with BIRC2 and treated with pifithrin-μ (an inhibitor of mitochondrial p53) or pifithrin-α (an inhibitor of p53 transactivation) were lower than those of larvae without pifithrin-μ or pifithrin-α treatment. Critically, the p53 inactivators pifithrin-μ and pifithrin-α had no significant effect on larval survival, but completely rescued larval survival for zebrafish microinjected with BIRC2 in the case of E. piscicida infection. Collectively, the present study suggest that piscine BIRC2 is a negative regulator for antibacterial immune response in response to the E. piscicida infection via inhibiting caspases, and accumulating p53 in a p53 transcription-dependent and -independent manner.

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Section: Discussionmentioning

confidence: 99%

The Zebrafish Antiapoptotic Protein BIRC2 Promotes Edwardsiella piscicida Infection by Inhibiting Caspases and Accumulating p53 in a p53 Transcription-Dependent and -Independent Manner

et al. 2021

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“…Several lines of evidence indicate that IAPs, and more generally endothelial cell apoptosis, are important for normal vascular development in mammals as well as zebrafish [104]. Endothelial cell apoptosis has been observed in mouse embryos beginning at E14.5 and inhibition of this process by the anti-apoptotic Bcl-2 protein results in abnormally dense and disorganized networks of small vessels [105].…”

Section: Zebrafish Iap Proteins and Iap Antagonistsmentioning

confidence: 98%

The zebrafish as a model organism for the study of apoptosis

2009

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Apoptosis plays important roles in embryogenesis, tissue homeostasis, and immune system regulation. The zebrafish (Danio rerio) is a powerful vertebrate model organism that has been extensively used to study apoptotic cell death during normal development and under conditions of cellular stress. In the past 5 years, a detailed picture has begun to emerge of the molecular underpinnings of the cell-intrinsic and the cell-extrinsic apoptosis signaling pathways in zebrafish. We begin this review with an introduction to the techniques and experimental approaches that are used to study apoptosis in zebrafish. We follow with a general overview of developmental apoptosis during zebrafish embryogenesis. Finally, we present a comprehensive review of the intrinsic and extrinsic apoptosis pathways in zebrafish, focusing on the high degree of conservation with humans and other mammals. Recent publications that draw upon the unique advantages of the zebrafish system to study novel aspects of apoptosis regulation and function are highlighted throughout.

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“…29,30 Different studies have highlighted a strong similarity between zebrafish and other animal models in basic molecular mechanisms of vascular development 29 and in particular in sprouting angiogenesis. 31,32 Nevertheless, the majority of these studies focused on ISVs formation and few of them drew attention to the mechanisms regulating CP formation.…”

Section: Synergistic Interaction Of β-Nrxn1a and Nlgn1 In Cp Formatiomentioning

confidence: 99%

The Synaptic Proteins β-Neurexin and Neuroligin Synergize With Extracellular Matrix-Binding Vascular Endothelial Growth Factor A During Zebrafish Vascular Development

Rissone

Foglia

Sangiorgio

et al. 2012

ATVB

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Objective— The goal of this study was to determine the in vivo functions of the synaptic proteins neurexins and neuroligins in embryonic vascular system development using zebrafish as animal model. Methods and Results— In the present study, we show that the knockdown of the α-form of neurexin 1a induces balance defects and reduced locomotory activity, whereas β-neurexin 1a and neuroligin 1 morphants present defects in sprouting angiogenesis and vascular remodeling, in particular in the caudal plexus and subintestinal vessels. Coinjection of low doses of morpholinos for β-neurexin 1a and neuroligin 1 together or in combination with morpholinos targeting the heparin-binding isoforms of vascular endothelial growth factor A (encoded by the VEGFAb gene) recapitulates the observed abnormalities, suggesting synergistic activity of these molecules. Similar coinjection experiments with morpholinos, targeting the enzyme heparan sulfate 6-O-sulfotransferase 2, confirm the presence of a functional correlation between extracellular matrix maturation and β-neurexin 1a or neuroligin 1. Conclusion— Our data represent the first in vivo evidence of the role of neurexin and neuroligin in embryonic blood vessel formation and provide insights into their mechanism of action

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Keeping your vascular integrity: What can we learn from fish?

Cited by 7 publications

References 40 publications

The Zebrafish Antiapoptotic Protein BIRC2 Promotes Edwardsiella piscicida Infection by Inhibiting Caspases and Accumulating p53 in a p53 Transcription-Dependent and -Independent Manner

The Zebrafish Antiapoptotic Protein BIRC2 Promotes Edwardsiella piscicida Infection by Inhibiting Caspases and Accumulating p53 in a p53 Transcription-Dependent and -Independent Manner

The zebrafish as a model organism for the study of apoptosis

The Synaptic Proteins β-Neurexin and Neuroligin Synergize With Extracellular Matrix-Binding Vascular Endothelial Growth Factor A During Zebrafish Vascular Development

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