Superoxide induces apoptosis in cardiomyocytes, but proliferation and expression of transforming growth factor-β1 in cardiac fibroblasts
Cardiomyocyte apoptosis and cardiac fibroblast proliferation are characteristic features of failing myocardium. Here we investigated the effect of superoxide on the cell fate of cardiomyocytes and cardiac fibroblasts. Cultured rat cardiomyocytes or cardiac fibroblasts were treated with superoxide. I...
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| Published in | FEBS letters Vol. 448; no. 2; pp. 206 - 210 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
Elsevier B.V
09.04.1999
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| Subjects | |
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| Abstract | Cardiomyocyte apoptosis and cardiac fibroblast proliferation are characteristic features of failing myocardium. Here we investigated the effect of superoxide on the cell fate of cardiomyocytes and cardiac fibroblasts. Cultured rat cardiomyocytes or cardiac fibroblasts were treated with superoxide. In response to superoxide stimulation cardiomyocytes underwent apoptosis as revealed by the increase in histone associated DNA fragmentation and positive to in situ nick end-labeling. In contrast, cardiac fibroblasts were stimulated to proliferate as demonstrated by the increase in DNA synthesis detected by [
3H]thymidine incorporation and in cell number. Additionally, Northern blot analysis showed that transforming growth factor-β1, a key factor responsible for myocardial fibrosis, was upregulated in cardiac fibroblasts in response to superoxide stimulation. These data suggest that superoxide can induce such divergent effects as apoptosis in cardiomyocytes and cell growth in cardiac fibroblasts, indicating that it may be a potential factor involved in the pathogenesis of heart failure. |
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| AbstractList | Cardiomyocyte apoptosis and cardiac fibroblast proliferation are characteristic features of failing myocardium. Here we investigated the effect of superoxide on the cell fate of cardiomyocytes and cardiac fibroblasts. Cultured rat cardiomyocytes or cardiac fibroblasts were treated with superoxide. In response to superoxide stimulation cardiomyocytes underwent apoptosis as revealed by the increase in histone associated DNA fragmentation and positive to in situ nick end‐labeling. In contrast, cardiac fibroblasts were stimulated to proliferate as demonstrated by the increase in DNA synthesis detected by [3H]thymidine incorporation and in cell number. Additionally, Northern blot analysis showed that transforming growth factor‐β1, a key factor responsible for myocardial fibrosis, was upregulated in cardiac fibroblasts in response to superoxide stimulation. These data suggest that superoxide can induce such divergent effects as apoptosis in cardiomyocytes and cell growth in cardiac fibroblasts, indicating that it may be a potential factor involved in the pathogenesis of heart failure. Cardiomyocyte apoptosis and cardiac fibroblast proliferation are characteristic features of failing myocardium. Here we investigated the effect of superoxide on the cell fate of cardiomyocytes and cardiac fibroblasts. Cultured rat cardiomyocytes or cardiac fibroblasts were treated with superoxide. In response to superoxide stimulation cardiomyocytes underwent apoptosis as revealed by the increase in histone associated DNA fragmentation and positive to in situ nick end‐labeling. In contrast, cardiac fibroblasts were stimulated to proliferate as demonstrated by the increase in DNA synthesis detected by [ 3 H]thymidine incorporation and in cell number. Additionally, Northern blot analysis showed that transforming growth factor‐β1, a key factor responsible for myocardial fibrosis, was upregulated in cardiac fibroblasts in response to superoxide stimulation. These data suggest that superoxide can induce such divergent effects as apoptosis in cardiomyocytes and cell growth in cardiac fibroblasts, indicating that it may be a potential factor involved in the pathogenesis of heart failure. Cardiomyocyte apoptosis and cardiac fibroblast proliferation are characteristic features of failing myocardium. Here we investigated the effect of superoxide on the cell fate of cardiomyocytes and cardiac fibroblasts. Cultured rat cardiomyocytes or cardiac fibroblasts were treated with superoxide. In response to superoxide stimulation cardiomyocytes underwent apoptosis as revealed by the increase in histone associated DNA fragmentation and positive to in situ nick end-labeling. In contrast, cardiac fibroblasts were stimulated to proliferate as demonstrated by the increase in DNA synthesis detected by [ 3H]thymidine incorporation and in cell number. Additionally, Northern blot analysis showed that transforming growth factor-β1, a key factor responsible for myocardial fibrosis, was upregulated in cardiac fibroblasts in response to superoxide stimulation. These data suggest that superoxide can induce such divergent effects as apoptosis in cardiomyocytes and cell growth in cardiac fibroblasts, indicating that it may be a potential factor involved in the pathogenesis of heart failure. |
| Author | von Harsdorf, Rüdiger Li, Pei-Feng Dietz, Rainer |
| Author_xml | – sequence: 1 givenname: Pei-Feng surname: Li fullname: Li, Pei-Feng – sequence: 2 givenname: Rainer surname: Dietz fullname: Dietz, Rainer – sequence: 3 givenname: Rüdiger surname: von Harsdorf fullname: von Harsdorf, Rüdiger |
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| Copyright | 1999 Federation of European Biochemical Societies FEBS Letters 448 (1999) 1873-3468 © 2015 Federation of European Biochemical Societies |
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| Keywords | TUNEL, terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling XO/X, xanthine oxidase plus xanthine TGF-β1, transforming growth factor-β1 Cardiomyocyte Cardiac fibroblast Superoxide Proliferation Apoptosis SOD, superoxide dismutase |
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| Snippet | Cardiomyocyte apoptosis and cardiac fibroblast proliferation are characteristic features of failing myocardium. Here we investigated the effect of superoxide... |
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| SubjectTerms | Apoptosis Cardiac fibroblast Cardiomyocyte Proliferation SOD, superoxide dismutase Superoxide TGF-β1, transforming growth factor-β1 TUNEL, terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling XO/X, xanthine oxidase plus xanthine |
| Title | Superoxide induces apoptosis in cardiomyocytes, but proliferation and expression of transforming growth factor-β1 in cardiac fibroblasts |
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