The Chromogranin A-derived sympathomimetic serpinin depresses myocardial performance in teleost and amphibian hearts

Imbrogno, Sandra; Mazza, Rosa; Pugliese, Chiara; Filice, Mariacristina; Angelone, Tommaso; Loh, Y Peng; Tota, Bruno; Cerra, Maria Carmela

doi:10.1016/j.ygcen.2016.09.004

Cited by 17 publications

(14 citation statements)

References 57 publications

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“…The ex vivo isolated and perfused goldfish heart showed basal values of preload, afterload, HR, CO, SV and SW (Table 1) comparable to those previously reported [normoxia: [8,28,36,38]; hypoxia: [8,12,38]].…”

Section: Isolated Heart Preparationssupporting

confidence: 87%

“…Mammalian cardiomyocytes express both nNOS [84] and eNOS [85], whose differential biological functions are tightly related to intracellular compartmentation, differences in their stimulation, and specific recruitment of distinct downstream transduction pathways (see [86] for references). In teleost fish, as well as in agnathans and chondrichthyans, while physio-pharmacological approaches and NADPH-diaphorase and immunolocalization studies have documented the presence of an "eNOS-like" activity in the heart of several species [28,[86][87][88], a gene for a canonical eNOS has been yet not identified (see for reference [86,89]). It has been proposed that in teleost, a nNOS isoform showing an endothelial-like consensus may cover some functional features of the eNOS isoform identity.…”

Section: Limitation Of the Studymentioning

confidence: 99%

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The Hypoxia Tolerance of the Goldfish (Carassius auratus) Heart: The NOS/NO System and Beyond

et al. 2020

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The extraordinary capacity of the goldfish (Carassius auratus) to increase its cardiac performance under acute hypoxia is crucial in ensuring adequate oxygen supply to tissues and organs. However, the underlying physiological mechanisms are not yet completely elucidated. By employing an ex vivo working heart preparation, we observed that the time-dependent enhancement of contractility, distinctive of the hypoxic goldfish heart, is abolished by the Nitric Oxide Synthase (NOS) antagonist L-NMMA, the Nitric Oxide (NO) scavenger PTIO, as well as by the PI3-kinase (PI3-K) and sarco/endoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) pumps’ inhibition by Wortmannin and Thapsigargin, respectively. In goldfish hearts exposed to hypoxia, an ELISA test revealed no changes in cGMP levels, while Western Blotting analysis showed an enhanced expression of the phosphorylated protein kinase B (pAkt) and of the NADPH oxidase catalytic subunit Nox2 (gp91phox). A significant decrease of protein S-nitrosylation was observed by Biotin Switch assay in hypoxic hearts. Results suggest a role for a PI3-K/Akt-mediated activation of the NOS-dependent NO production, and SERCA2a pumps in the mechanisms conferring benefits to the goldfish heart under hypoxia. They also propose protein denitrosylation, and the possibility of nitration, as parallel intracellular events.

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Section: Isolated Heart Preparationssupporting

confidence: 87%

Section: Limitation Of the Studymentioning

confidence: 99%

The Hypoxia Tolerance of the Goldfish (Carassius auratus) Heart: The NOS/NO System and Beyond

et al. 2020

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“…Another similarity with mammals (Rocca et al, 2018a) is the involvement of pAkt in the intracellular mechanism of action elicited by PSELT in the goldfish heart. The recruitment of the cAMP/PKA pathway, L-type calcium channels and SERCA2a pumps for positive inotropism of PSELT suggests that the peptide acts on the goldfish myocardium via the modulation of intracellular pathways involved in the control of fish basal myocardial performance (Garofalo et al, 2009(Garofalo et al, , 2015Imbrogno et al, 2017). The present data from fish propose SELENOT as an ancient positive inotropic agent that can also be regarded as a putative new effector in the complex mechanism of hypoxia resistance of the goldfish heart, currently only partially uncovered.…”

Section: Discussionmentioning

confidence: 75%

Selenoprotein T as a new positive inotrope in the goldfish Carassius auratus

Mazza

Gattuso

Imbrogno

et al. 2019

Journal of Experimental Biology

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Selenoprotein T (SELENOT) is a thioredoxin-like protein, which mediates oxidoreductase functions via its redox active motif Cys-X-X-Sec. In mammals, SELENOT is expressed during ontogenesis and progressively decreases in adult tissues. In the heart, it is re-expressed after ischemia and induces cardioprotection against ischemia-reperfusion (IR) injury. SELENOT is present in teleost fish, including the goldfish Carassius auratus. This study aimed to evaluate the cardiac expression of SELENOT, and the effects of exogenous PSELT (a 43-52 SELENOT-derived peptide) on the heart function of C. auratus, a hypoxia tolerance fish model. We found that SELENOT was expressed in cardiac extracts of juvenile and adult fish, located in the sarcoplasmic reticulum (SR) together with calsequestrin-2. Expression increased under acute hypoxia. On ex vivo isolated and perfused goldfish heart preparations, under normoxia, PSELT dose dependently increased stroke volume (V S), cardiac output ð _ QÞ and stroke work (SW), involving cAMP, PKA, L-type calcium channels, SERCA2a pumps and pAkt. Under hypoxia, PSELT did not affect myocardial contractility. Only at higher concentrations (10 −8 to 10 −7 mol l −1) was an increase of V S and _ Q observed. It also reduced the cardiac expression of 3-NT, a tissue marker of nitrosative stress, which increases under low oxygen availability. These data are the first to propose SELENOT 43-52 (PSELT) as a cardiac modulator in fish, with a potential protective role under hypoxia.

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“…In fish, the role of NO as a major organizer of complex cardiac transduction signals has been widely assessed, and to date many data are available about its wide cardiac repertoire of actions (see for example Garofalo et al, 2009a , 2012 ; Imbrogno et al, 2010 , 2013 , 2017 , 2018 ; Filice et al, 2017 ; Imbrogno and Cerra, 2017 ). Very recent studies extended the large variety of NO functions in fish to the mechanisms which allow to maintain the cardiovascular status and control the response to low O 2 .…”

Section: Cardiac Nitrosative Signalsmentioning

confidence: 99%

Hypoxia Tolerance in Teleosts: Implications of Cardiac Nitrosative Signals

Gattuso¹,

Garofalo²,

Cerra³

et al. 2018

Front. Physiol.

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Changes in environmental oxygen (O2) are naturally occurring phenomena which ectotherms have to face on. Many species exhibit a striking capacity to survive and remain active for long periods under hypoxia, even tolerating anoxia. Some fundamental adaptations contribute to this capacity: metabolic suppression, tolerance of pH and ionic unbalance, avoidance and/or repair of free-radical-induced cell injury during reoxygenation. A remarkable feature of these species is their ability to preserve a normal cardiovascular performance during hypoxia/anoxia to match peripheral (tissue pO2) requirements. In this review, we will refer to paradigms of hypoxia- and anoxia-tolerant teleost fish to illustrate cardiac physiological strategies that, by involving nitric oxide and its metabolites, play a critical role in the adaptive responses to O2 limitation. The information here reported may contribute to clarify the molecular and cellular mechanisms underlying heart vulnerability vs. resistance in relation to O2 availability.

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The Chromogranin A-derived sympathomimetic serpinin depresses myocardial performance in teleost and amphibian hearts

Cited by 17 publications

References 57 publications

The Hypoxia Tolerance of the Goldfish (Carassius auratus) Heart: The NOS/NO System and Beyond

The Hypoxia Tolerance of the Goldfish (Carassius auratus) Heart: The NOS/NO System and Beyond

Selenoprotein T as a new positive inotrope in the goldfish Carassius auratus

Hypoxia Tolerance in Teleosts: Implications of Cardiac Nitrosative Signals

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