The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and Beyond
The extraordinary capacity of the goldfish (<i>Carassius auratus</i>) 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 employ...
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| Format: | Article |
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MDPI AG
2020-06-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/9/6/555 |
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| author | Mariacristina Filice Rosa Mazza Serena Leo Alfonsina Gattuso Maria Carmela Cerra Sandra Imbrogno |
| author_facet | Mariacristina Filice Rosa Mazza Serena Leo Alfonsina Gattuso Maria Carmela Cerra Sandra Imbrogno |
| author_sort | Mariacristina Filice |
| collection | DOAJ |
| description | The extraordinary capacity of the goldfish (<i>Carassius auratus</i>) 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 Ca<sup>2+</sup>-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. |
| first_indexed | 2024-03-10T18:52:52Z |
| format | Article |
| id | doaj.art-f7e5192118fe4663834b769064209754 |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-10T18:52:52Z |
| publishDate | 2020-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-f7e5192118fe4663834b7690642097542023-11-20T05:02:52ZengMDPI AGAntioxidants2076-39212020-06-019655510.3390/antiox9060555The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and BeyondMariacristina Filice0Rosa Mazza1Serena Leo2Alfonsina Gattuso3Maria Carmela Cerra4Sandra Imbrogno5Department of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Arcavacata di Rende (CS), ItalyDepartment of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Arcavacata di Rende (CS), ItalyDepartment of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Arcavacata di Rende (CS), ItalyDepartment of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Arcavacata di Rende (CS), ItalyDepartment of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Arcavacata di Rende (CS), ItalyDepartment of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Arcavacata di Rende (CS), ItalyThe extraordinary capacity of the goldfish (<i>Carassius auratus</i>) 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 Ca<sup>2+</sup>-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.https://www.mdpi.com/2076-3921/9/6/555myocardial performancecGMPSERCA2aNox2nitrosative signals |
| spellingShingle | Mariacristina Filice Rosa Mazza Serena Leo Alfonsina Gattuso Maria Carmela Cerra Sandra Imbrogno The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and Beyond Antioxidants myocardial performance cGMP SERCA2a Nox2 nitrosative signals |
| title | The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and Beyond |
| title_full | The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and Beyond |
| title_fullStr | The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and Beyond |
| title_full_unstemmed | The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and Beyond |
| title_short | The Hypoxia Tolerance of the Goldfish (<i>Carassius auratus</i>) Heart: The NOS/NO System and Beyond |
| title_sort | hypoxia tolerance of the goldfish i carassius auratus i heart the nos no system and beyond |
| topic | myocardial performance cGMP SERCA2a Nox2 nitrosative signals |
| url | https://www.mdpi.com/2076-3921/9/6/555 |
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