Inhibition of let-7c Regulates Cardiac Regeneration after Cryoinjury in Adult Zebrafish

Narumanchi, Suneeta; Kalervo, Karri; Perttunen, Sanni; Wang, Hong; Immonen, Katariina; Kosonen, Riikka; Laine, Mika; Ruskoaho, Heikki; Tikkanen, Ilkka; Lakkisto, Päivi; Paavola, Jere

doi:10.3390/jcdd6020016

Cited by 6 publications

(3 citation statements)

References 45 publications

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“…Fractional shortening may be measured 1- (diameter), 2- (area), or 3- (volume) dimensionally. In adult zebrafish, we found fractional volume shortening to be the most reliable method ( Narumanchi et al, 2019 ). From the same fast frame-rate recordings, cardiac relaxation time may be measured ( Paavola et al, 2020 ).…”

Section: Defining Heart Failure In Zebrafishmentioning

confidence: 99%

Zebrafish Heart Failure Models

Narumanchi

Wang

Perttunen

et al. 2021

Front. Cell Dev. Biol.

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Heart failure causes significant morbidity and mortality worldwide. The understanding of heart failure pathomechanisms and options for treatment remain incomplete. Zebrafish has proven useful for modeling human heart diseases due to similarity of zebrafish and mammalian hearts, fast easily tractable development, and readily available genetic methods. Embryonic cardiac development is rapid and cardiac function is easy to observe and quantify. Reverse genetics, by using morpholinos and CRISPR-Cas9 to modulate gene function, make zebrafish a primary animal model for in vivo studies of candidate genes. Zebrafish are able to effectively regenerate their hearts following injury. However, less attention has been given to using zebrafish models to increase understanding of heart failure and cardiac remodeling, including cardiac hypertrophy and hyperplasia. Here we discuss using zebrafish to study heart failure and cardiac remodeling, and review zebrafish genetic, drug-induced and other heart failure models, discussing the advantages and weaknesses of using zebrafish to model human heart disease. Using zebrafish models will lead to insights on the pathomechanisms of heart failure, with the aim to ultimately provide novel therapies for the prevention and treatment of heart failure.

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Section: Defining Heart Failure In Zebrafishmentioning

confidence: 99%

Zebrafish Heart Failure Models

Narumanchi

Wang

Perttunen

et al. 2021

Front. Cell Dev. Biol.

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“…The progression from the fibrin clot to the regenerated apex at day 60 may then be studied ( Figure 3 ). Of specific interest in the field of heart regeneration, cardiomyocyte proliferation may be evaluated in this set-up by merging it with other staining, e.g., against nuclear markers of cardiomyocytes like Mef2 [ 6 ] or the proliferating cell nuclear antigen (PCNA) [ 6 , 26 ]. Alternatively, 5-Ethynyl-2′-deoxyuridine (EdU) may be pulse-chased in the living zebrafish to analyse DNA synthesis in dividing cells [ 27 ] and then visualized afterwards by staining.…”

Section: Resultsmentioning

confidence: 99%

Apex Resection in Zebrafish (Danio rerio) as a Model of Heart Regeneration: A Video-Assisted Guide

Ellman

Slaiman

Mathiesen

et al. 2021

IJMS

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Ischemic heart disease is one of the leading causes of deaths worldwide. A major hindrance to resolving this challenge lies in the mammalian hearts inability to regenerate after injury. In contrast, zebrafish retain a regenerative capacity of the heart throughout their lifetimes. Apex resection (AR) is a popular zebrafish model for studying heart regeneration, and entails resecting 10–20% of the heart in the apex region, whereafter the regeneration process is monitored until the heart is fully regenerated within 60 days. Despite this popularity, video tutorials describing this technique in detail are lacking. In this paper we visualize and describe the entire AR procedure including anaesthesia, surgery, and recovery. In addition, we show that the concentration and duration of anaesthesia are important parameters to consider, to balance sufficient levels of sedation and minimizing mortality. Moreover, we provide examples of how zebrafish heart regeneration can be assessed both in 2D (immunohistochemistry of heart sections) and 3D (analyses of whole, tissue cleared hearts using multiphoton imaging). In summary, this paper aims to aid beginners in establishing and conducting the AR model in their laboratory, but also to spur further interest in improving the model and its evaluation.

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“…Echocardiographic images were acquired in the longitudinal axis (LAX) view to record B-mode videos and in the short axis (SAX) view to obtain pulsed-wave Doppler (PWD) signals. Image analysis was conducted offline using Vevo Lab™ analysis software (VisualSonics) by experienced personnel in a blinded manner as described recently [ 57 ]. Briefly, ventricular longitudinal diameters from five consecutive cardiac cycles were obtained from B-mode images by measuring the perpendicular distance from the base to the apex at end-diastole (EDD) and end-systole (ESD).…”

Section: Methodsmentioning

confidence: 99%

Tankyrase Inhibition Attenuates Cardiac Dilatation and Dysfunction in Ischemic Heart Failure

Wang

Segersvärd

Siren

et al. 2022

IJMS

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Hyperactive poly(ADP-ribose) polymerases (PARP) promote ischemic heart failure (IHF) after myocardial infarction (MI). However, the role of tankyrases (TNKSs), members of the PARP family, in pathogenesis of IHF remains unknown. We investigated the expression and activation of TNKSs in myocardium of IHF patients and MI rats. We explored the cardioprotective effect of TNKS inhibition in an isoproterenol-induced zebrafish HF model. In IHF patients, we observed elevated TNKS2 and DICER and concomitant upregulation of miR-34a-5p and miR-21-5p in non-infarcted myocardium. In a rat MI model, we found augmented TNKS2 and DICER in the border and infarct areas at the early stage of post-MI. We also observed consistently increased TNKS1 in the border and infarct areas and destabilized AXIN in the infarct area from 4 weeks onward, which in turn triggered Wnt/β-catenin signaling. In an isoproterenol-induced HF zebrafish model, inhibition of TNKS activity with XAV939, a TNKSs-specific inhibitor, protected against ventricular dilatation and cardiac dysfunction and abrogated overactivation of Wnt/β-catenin signaling and dysregulation of miR-34a-5p induced by isoproterenol. Our study unravels a potential role of TNKSs in the pathogenesis of IHF by regulating Wnt/β-catenin signaling and possibly modulating miRNAs and highlights the pharmacotherapeutic potential of TNKS inhibition for prevention of IHF.

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Inhibition of let-7c Regulates Cardiac Regeneration after Cryoinjury in Adult Zebrafish

Cited by 6 publications

References 45 publications

Zebrafish Heart Failure Models

Zebrafish Heart Failure Models

Apex Resection in Zebrafish (Danio rerio) as a Model of Heart Regeneration: A Video-Assisted Guide

Tankyrase Inhibition Attenuates Cardiac Dilatation and Dysfunction in Ischemic Heart Failure

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