Cardiac Left Ventricle Mitochondrial Dysfunction After Neonatal Exposure to Hyperoxia: Relevance for Cardiomyopathy After Preterm Birth
Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized...
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| Published in | Hypertension (Dallas, Tex. 1979) Vol. 79; no. 3; pp. 575 - 587 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Lippincott Williams & Wilkins
01.03.2022
American Heart Association |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0194-911X 1524-4563 1524-4563 |
| DOI | 10.1161/HYPERTENSIONAHA.121.17979 |
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| Abstract | Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm.
Sprague-Dawley pups were exposed to room air (controls) or 80% O
at postnatal days 3 to 10 (oxygen-induced cardiomyopathy). We studied left ventricle mitochondrial changes in 4 weeks old males. In a cohort of young adults born preterm (n=55) and age-matched term (n=54), we compared circulating levels of humanin.
Compared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced
gene expression. In the cohort, left ventricle ejection fraction and peak global longitudinal strain were similar between groups however humanin levels were lower in preterm and associated with left ventricle ejection fraction and peak global longitudinal strain.
In conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609. |
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| AbstractList | Supplemental Digital Content is available in the text.
Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm. Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm. Sprague-Dawley pups were exposed to room air (controls) or 80% O at postnatal days 3 to 10 (oxygen-induced cardiomyopathy). We studied left ventricle mitochondrial changes in 4 weeks old males. In a cohort of young adults born preterm (n=55) and age-matched term (n=54), we compared circulating levels of humanin. Compared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced gene expression. In the cohort, left ventricle ejection fraction and peak global longitudinal strain were similar between groups however humanin levels were lower in preterm and associated with left ventricle ejection fraction and peak global longitudinal strain. In conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609. Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm.BACKGROUNDIndividuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm.Sprague-Dawley pups were exposed to room air (controls) or 80% O2 at postnatal days 3 to 10 (oxygen-induced cardiomyopathy). We studied left ventricle mitochondrial changes in 4 weeks old males. In a cohort of young adults born preterm (n=55) and age-matched term (n=54), we compared circulating levels of humanin.METHODSSprague-Dawley pups were exposed to room air (controls) or 80% O2 at postnatal days 3 to 10 (oxygen-induced cardiomyopathy). We studied left ventricle mitochondrial changes in 4 weeks old males. In a cohort of young adults born preterm (n=55) and age-matched term (n=54), we compared circulating levels of humanin.Compared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced Nrf2 gene expression. In the cohort, left ventricle ejection fraction and peak global longitudinal strain were similar between groups however humanin levels were lower in preterm and associated with left ventricle ejection fraction and peak global longitudinal strain.RESULTSCompared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced Nrf2 gene expression. In the cohort, left ventricle ejection fraction and peak global longitudinal strain were similar between groups however humanin levels were lower in preterm and associated with left ventricle ejection fraction and peak global longitudinal strain.In conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609.CONCLUSIONSIn conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609. Background: Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm. Methods: Sprague-Dawley pups were exposed to room air (controls) or 80% O 2 at postnatal days 3 to 10 (oxygen-induced cardiomyopathy). We studied left ventricle mitochondrial changes in 4 weeks old males. In a cohort of young adults born preterm (n=55) and age-matched term (n=54), we compared circulating levels of humanin. Results: Compared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced Nrf2 gene expression. In the cohort, left ventricle ejection fraction and peak global longitudinal strain were similar between groups however humanin levels were lower in preterm and associated with left ventricle ejection fraction and peak global longitudinal strain. Conclusions: In conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth–related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03261609. |
| Author | Deprez, Alyson Flahault, Adrien Pontes, Carolina N.R. Burelle, Yan Gaub, Perrine Mai Luu, Thuy Altit, Gabriel Joyal, Jean-Sébastien Nuyt, Anne Monique Bigras, Jean-Luc He, Ying Cloutier, Anik Cagnone, Gaël Ravizzoni Dartora, Daniela |
| AuthorAffiliation | Division of Neonatology, Department of Pediatrics, Montreal Children’s Hospital, McGill University, Montreal, Quebec, Canada (G.A.) Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada Department of Cellular and Molecular Medicine, University of Ottawa, Canada (Y.B.) |
| AuthorAffiliation_xml | – name: Department of Cellular and Molecular Medicine, University of Ottawa, Canada (Y.B.) – name: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – name: Division of Neonatology, Department of Pediatrics, Montreal Children’s Hospital, McGill University, Montreal, Quebec, Canada (G.A.) |
| Author_xml | – sequence: 1 givenname: Daniela surname: Ravizzoni Dartora fullname: Ravizzoni Dartora, Daniela organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 2 givenname: Adrien surname: Flahault fullname: Flahault, Adrien organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 3 givenname: Carolina N.R. surname: Pontes fullname: Pontes, Carolina N.R. organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 4 givenname: Ying surname: He fullname: He, Ying organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 5 givenname: Alyson surname: Deprez fullname: Deprez, Alyson organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 6 givenname: Anik surname: Cloutier fullname: Cloutier, Anik organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 7 givenname: Gaël surname: Cagnone fullname: Cagnone, Gaël organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 8 givenname: Perrine surname: Gaub fullname: Gaub, Perrine organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 9 givenname: Gabriel surname: Altit fullname: Altit, Gabriel organization: Division of Neonatology, Department of Pediatrics, Montreal Children’s Hospital, McGill University, Montreal, Quebec, Canada (G.A.) – sequence: 10 givenname: Jean-Luc surname: Bigras fullname: Bigras, Jean-Luc organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 11 givenname: Jean-Sébastien surname: Joyal fullname: Joyal, Jean-Sébastien organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 12 givenname: Thuy surname: Mai Luu fullname: Mai Luu, Thuy organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada – sequence: 13 givenname: Yan surname: Burelle fullname: Burelle, Yan organization: Department of Cellular and Molecular Medicine, University of Ottawa, Canada (Y.B.) – sequence: 14 givenname: Anne Monique surname: Nuyt fullname: Nuyt, Anne Monique organization: Department of Pediatrics, Sainte-Justine University Hospital (Centre Hospitalier Universitaire Sainte-Justine) and Research Centre (D.R.D., A.F., C.N.R.P., Y.H., A.D., A.C., G.C., P.G., J.-L.B., J.-S.J., T.M.L., A.M.N.), Faculty of Medicine, University of Montreal, Quebec, Canada |
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| Snippet | Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after... Background: Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart... Supplemental Digital Content is available in the text. Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart... |
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| SubjectTerms | Adolescent Adult Animals Cardiology and cardiovascular system Cardiomyopathies Cardiomyopathies - etiology Cardiomyopathies - metabolism Cardiomyopathies - physiopathology Female Human health and pathology Humans Hyperoxia Hyperoxia - complications Hyperoxia - metabolism Hyperoxia - physiopathology Intracellular Signaling Peptides and Proteins Intracellular Signaling Peptides and Proteins - blood Life Sciences Male Mitochondria Mitochondria - metabolism Myocytes, Cardiac Myocytes, Cardiac - metabolism Original Oxidative Phosphorylation Pediatrics Premature Birth Rats Rats, Sprague-Dawley Ventricular Dysfunction, Left Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - physiopathology Young Adult |
| Title | Cardiac Left Ventricle Mitochondrial Dysfunction After Neonatal Exposure to Hyperoxia: Relevance for Cardiomyopathy After Preterm Birth |
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