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Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health
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| Zeitschriftentitel: | Scientific Reports |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , , , , , , , |
| In: | Scientific Reports, 7, 2017, 1 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Springer Science and Business Media LLC
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| Schlagwörter: |
| author_facet |
Heid, Johanna Cencioni, Chiara Ripa, Roberto Baumgart, Mario Atlante, Sandra Milano, Giuseppina Scopece, Alessandro Kuenne, Carsten Guenther, Stefan Azzimato, Valerio Farsetti, Antonella Rossi, Giacomo Braun, Thomas Pompilio, Giulio Martelli, Fabio Zeiher, Andreas M. Cellerino, Alessandro Gaetano, Carlo Spallotta, Francesco Heid, Johanna Cencioni, Chiara Ripa, Roberto Baumgart, Mario Atlante, Sandra Milano, Giuseppina Scopece, Alessandro Kuenne, Carsten Guenther, Stefan Azzimato, Valerio Farsetti, Antonella Rossi, Giacomo Braun, Thomas Pompilio, Giulio Martelli, Fabio Zeiher, Andreas M. Cellerino, Alessandro Gaetano, Carlo Spallotta, Francesco |
|---|---|
| author |
Heid, Johanna Cencioni, Chiara Ripa, Roberto Baumgart, Mario Atlante, Sandra Milano, Giuseppina Scopece, Alessandro Kuenne, Carsten Guenther, Stefan Azzimato, Valerio Farsetti, Antonella Rossi, Giacomo Braun, Thomas Pompilio, Giulio Martelli, Fabio Zeiher, Andreas M. Cellerino, Alessandro Gaetano, Carlo Spallotta, Francesco |
| spellingShingle |
Heid, Johanna Cencioni, Chiara Ripa, Roberto Baumgart, Mario Atlante, Sandra Milano, Giuseppina Scopece, Alessandro Kuenne, Carsten Guenther, Stefan Azzimato, Valerio Farsetti, Antonella Rossi, Giacomo Braun, Thomas Pompilio, Giulio Martelli, Fabio Zeiher, Andreas M. Cellerino, Alessandro Gaetano, Carlo Spallotta, Francesco Scientific Reports Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health Multidisciplinary |
| author_sort |
heid, johanna |
| spelling |
Heid, Johanna Cencioni, Chiara Ripa, Roberto Baumgart, Mario Atlante, Sandra Milano, Giuseppina Scopece, Alessandro Kuenne, Carsten Guenther, Stefan Azzimato, Valerio Farsetti, Antonella Rossi, Giacomo Braun, Thomas Pompilio, Giulio Martelli, Fabio Zeiher, Andreas M. Cellerino, Alessandro Gaetano, Carlo Spallotta, Francesco 2045-2322 Springer Science and Business Media LLC Multidisciplinary http://dx.doi.org/10.1038/s41598-017-16829-w <jats:title>Abstract</jats:title><jats:p>The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12–21 week (adult) and 28–40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O<jats:sub>2</jats:sub> levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.</jats:p> Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health Scientific Reports |
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| title |
Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_unstemmed |
Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_full |
Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_fullStr |
Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_full_unstemmed |
Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_short |
Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_sort |
age-dependent increase of oxidative stress regulates microrna-29 family preserving cardiac health |
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Multidisciplinary |
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http://dx.doi.org/10.1038/s41598-017-16829-w |
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2017 |
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<jats:title>Abstract</jats:title><jats:p>The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12–21 week (adult) and 28–40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O<jats:sub>2</jats:sub> levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.</jats:p> |
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| author | Heid, Johanna, Cencioni, Chiara, Ripa, Roberto, Baumgart, Mario, Atlante, Sandra, Milano, Giuseppina, Scopece, Alessandro, Kuenne, Carsten, Guenther, Stefan, Azzimato, Valerio, Farsetti, Antonella, Rossi, Giacomo, Braun, Thomas, Pompilio, Giulio, Martelli, Fabio, Zeiher, Andreas M., Cellerino, Alessandro, Gaetano, Carlo, Spallotta, Francesco |
| author_facet | Heid, Johanna, Cencioni, Chiara, Ripa, Roberto, Baumgart, Mario, Atlante, Sandra, Milano, Giuseppina, Scopece, Alessandro, Kuenne, Carsten, Guenther, Stefan, Azzimato, Valerio, Farsetti, Antonella, Rossi, Giacomo, Braun, Thomas, Pompilio, Giulio, Martelli, Fabio, Zeiher, Andreas M., Cellerino, Alessandro, Gaetano, Carlo, Spallotta, Francesco, Heid, Johanna, Cencioni, Chiara, Ripa, Roberto, Baumgart, Mario, Atlante, Sandra, Milano, Giuseppina, Scopece, Alessandro, Kuenne, Carsten, Guenther, Stefan, Azzimato, Valerio, Farsetti, Antonella, Rossi, Giacomo, Braun, Thomas, Pompilio, Giulio, Martelli, Fabio, Zeiher, Andreas M., Cellerino, Alessandro, Gaetano, Carlo, Spallotta, Francesco |
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| description | <jats:title>Abstract</jats:title><jats:p>The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12–21 week (adult) and 28–40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O<jats:sub>2</jats:sub> levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.</jats:p> |
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| spelling | Heid, Johanna Cencioni, Chiara Ripa, Roberto Baumgart, Mario Atlante, Sandra Milano, Giuseppina Scopece, Alessandro Kuenne, Carsten Guenther, Stefan Azzimato, Valerio Farsetti, Antonella Rossi, Giacomo Braun, Thomas Pompilio, Giulio Martelli, Fabio Zeiher, Andreas M. Cellerino, Alessandro Gaetano, Carlo Spallotta, Francesco 2045-2322 Springer Science and Business Media LLC Multidisciplinary http://dx.doi.org/10.1038/s41598-017-16829-w <jats:title>Abstract</jats:title><jats:p>The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12–21 week (adult) and 28–40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O<jats:sub>2</jats:sub> levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.</jats:p> Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health Scientific Reports |
| spellingShingle | Heid, Johanna, Cencioni, Chiara, Ripa, Roberto, Baumgart, Mario, Atlante, Sandra, Milano, Giuseppina, Scopece, Alessandro, Kuenne, Carsten, Guenther, Stefan, Azzimato, Valerio, Farsetti, Antonella, Rossi, Giacomo, Braun, Thomas, Pompilio, Giulio, Martelli, Fabio, Zeiher, Andreas M., Cellerino, Alessandro, Gaetano, Carlo, Spallotta, Francesco, Scientific Reports, Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health, Multidisciplinary |
| title | Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_full | Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_fullStr | Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_full_unstemmed | Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_short | Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| title_sort | age-dependent increase of oxidative stress regulates microrna-29 family preserving cardiac health |
| title_unstemmed | Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health |
| topic | Multidisciplinary |
| url | http://dx.doi.org/10.1038/s41598-017-16829-w |