Oxidative Stress-Induced Afterdepolarizations and Protein Kinase C Signaling
Background: Hydrogen peroxide (H2O2)-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an importan...
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| Published in | International journal of molecular sciences Vol. 18; no. 4; p. 688 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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01.04.2017
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| ISSN | 1422-0067 1661-6596 1422-0067 |
| DOI | 10.3390/ijms18040688 |
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| Abstract | Background: Hydrogen peroxide (H2O2)-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations. Methods: Action potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H2O2 (1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Gö 6983 (1 μM), was applied to test the involvement of PKC. Results: H2O2 perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Gö 6983 prevented the emergence of H2O2-induced afterdepolarizations. Additional application of Gö 6983 with H2O2 effectively suppressed H2O2-induced afterdepolarizations. H2O2 increased the late sodium current (INa,L) (n = 7, p < 0.01) and the L-type calcium current (ICa,L) (n = 5, p < 0.01), which were significantly reversed by Gö 6983 (p < 0.01). H2O2 also increased the transient outward potassium current (Ito) (n = 6, p < 0.05). However, Gö 6983 showed little effect on H2O2-induced enhancement of Ito. Conclusions: H2O2 induced afterdepolarizations via the activation of PKC and the enhancement of ICa,L and INa,L. These results provide evidence of a link between oxidative stress, PKC activation and afterdepolarizations. |
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| AbstractList | Background: Hydrogen peroxide (H2O2)-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations. Methods: Action potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H2O2 (1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Gö 6983 (1 μM), was applied to test the involvement of PKC. Results: H2O2 perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Gö 6983 prevented the emergence of H2O2-induced afterdepolarizations. Additional application of Gö 6983 with H2O2 effectively suppressed H2O2-induced afterdepolarizations. H2O2 increased the late sodium current (INa,L) (n = 7, p < 0.01) and the L-type calcium current (ICa,L) (n = 5, p < 0.01), which were significantly reversed by Gö 6983 (p < 0.01). H2O2 also increased the transient outward potassium current (Ito) (n = 6, p < 0.05). However, Gö 6983 showed little effect on H2O2-induced enhancement of Ito. Conclusions: H2O2 induced afterdepolarizations via the activation of PKC and the enhancement of ICa,L and INa,L. These results provide evidence of a link between oxidative stress, PKC activation and afterdepolarizations. Background: Hydrogen peroxide (H sub(2) O sub(2))-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations. Methods: Action potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H sub(2) O sub(2)(1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Go 6983 (1 [mu]M), was applied to test the involvement of PKC. Results: H sub(2) O sub(2) perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Go 6983 prevented the emergence of H sub(2) O sub(2)-induced afterdepolarizations. Additional application of Go 6983 with H sub(2) O sub(2) effectively suppressed H sub(2) O sub(2)-induced afterdepolarizations. H sub(2) O sub(2) increased the late sodium current (I sub(Na,L)) (n= 7, p< 0.01) and the L-type calcium current (I sub(Ca,L)) (n= 5, p< 0.01), which were significantly reversed by Go 6983 (p< 0.01). H sub(2) O sub(2) also increased the transient outward potassium current (I sub(to)) (n= 6, p< 0.05). However, Go 6983 showed little effect on H sub(2) O sub(2)-induced enhancement of I sub(to). Conclusions: H sub(2) O sub(2) induced afterdepolarizations via the activation of PKC and the enhancement of I sub(Ca,L) and I sub(Na,L). These results provide evidence of a link between oxidative stress, PKC activation and afterdepolarizations. Background: Hydrogen peroxide (H 2 O 2 )-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations. Methods: Action potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H 2 O 2 (1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Gö 6983 (1 μM), was applied to test the involvement of PKC. Results: H 2 O 2 perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Gö 6983 prevented the emergence of H 2 O 2 -induced afterdepolarizations. Additional application of Gö 6983 with H 2 O 2 effectively suppressed H 2 O 2 -induced afterdepolarizations. H 2 O 2 increased the late sodium current (I Na,L ) ( n = 7, p < 0.01) and the L-type calcium current (I Ca,L ) ( n = 5, p < 0.01), which were significantly reversed by Gö 6983 ( p < 0.01). H 2 O 2 also increased the transient outward potassium current (I to ) ( n = 6, p < 0.05). However, Gö 6983 showed little effect on H 2 O 2 -induced enhancement of I to . Conclusions: H 2 O 2 induced afterdepolarizations via the activation of PKC and the enhancement of I Ca,L and I Na,L . These results provide evidence of a link between oxidative stress, PKC activation and afterdepolarizations. Hydrogen peroxide (H₂O₂)-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations. Action potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H₂O₂ (1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Gö 6983 (1 μM), was applied to test the involvement of PKC. H₂O₂ perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Gö 6983 prevented the emergence of H₂O₂-induced afterdepolarizations. Additional application of Gö 6983 with H₂O₂ effectively suppressed H₂O₂-induced afterdepolarizations. H₂O₂ increased the late sodium current (I ) ( = 7, < 0.01) and the L-type calcium current (I ) ( = 5, < 0.01), which were significantly reversed by Gö 6983 ( < 0.01). H₂O₂ also increased the transient outward potassium current (I ) ( = 6, < 0.05). However, Gö 6983 showed little effect on H₂O₂-induced enhancement of I . H₂O₂ induced afterdepolarizations via the activation of PKC and the enhancement of I and I . These results provide evidence of a link between oxidative stress, PKC activation and afterdepolarizations. Hydrogen peroxide (H₂O₂)-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations.BACKGROUNDHydrogen peroxide (H₂O₂)-induced oxidative stress has been demonstrated to induce afterdepolarizations and triggered activities in isolated myocytes, but the underlying mechanisms remain not fully understood. We aimed to explore whether protein kinase C (PKC) activation plays an important role in oxidative stress-induced afterdepolarizations.Action potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H₂O₂ (1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Gö 6983 (1 μM), was applied to test the involvement of PKC.METHODSAction potentials and ion currents of isolated rabbit cardiomyocytes were recorded using the patch clamp technique. H₂O₂ (1 mM) was perfused to induce oxidative stress and the specific classical PKC inhibitor, Gö 6983 (1 μM), was applied to test the involvement of PKC.H₂O₂ perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Gö 6983 prevented the emergence of H₂O₂-induced afterdepolarizations. Additional application of Gö 6983 with H₂O₂ effectively suppressed H₂O₂-induced afterdepolarizations. H₂O₂ increased the late sodium current (INa,L) (n = 7, p < 0.01) and the L-type calcium current (ICa,L) (n = 5, p < 0.01), which were significantly reversed by Gö 6983 (p < 0.01). H₂O₂ also increased the transient outward potassium current (Ito) (n = 6, p < 0.05). However, Gö 6983 showed little effect on H₂O₂-induced enhancement of Ito.RESULTSH₂O₂ perfusion prolonged the action potential duration and induced afterdepolarizations. Pretreatment with Gö 6983 prevented the emergence of H₂O₂-induced afterdepolarizations. Additional application of Gö 6983 with H₂O₂ effectively suppressed H₂O₂-induced afterdepolarizations. H₂O₂ increased the late sodium current (INa,L) (n = 7, p < 0.01) and the L-type calcium current (ICa,L) (n = 5, p < 0.01), which were significantly reversed by Gö 6983 (p < 0.01). H₂O₂ also increased the transient outward potassium current (Ito) (n = 6, p < 0.05). However, Gö 6983 showed little effect on H₂O₂-induced enhancement of Ito.H₂O₂ induced afterdepolarizations via the activation of PKC and the enhancement of ICa,L and INa,L. These results provide evidence of a link between oxidative stress, PKC activation and afterdepolarizations.CONCLUSIONSH₂O₂ induced afterdepolarizations via the activation of PKC and the enhancement of ICa,L and INa,L. These results provide evidence of a link between oxidative stress, PKC activation and afterdepolarizations. |
| Author | Xu, Xiao-Lei Hou, Jian-Wen Fei, Yu-Dong Li, Wei Wang, Qian Guo, Kai Chen, Xiao-Meng Chen, Yi-He Wang, Yue-Peng Li, Yi-Gang |
| AuthorAffiliation | 1 Department of Cardiology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China; fyd6254@gmail.com (Y.-D.F.); lwcbss@163.com (W.L.); houjianwena@126.com (J.-W.H.); guokai0201@aliyun.com (K.G.); chenxmcorrine@outlook.com (X.-M.C.); cyh1726@163.com (Y.-H.C.); wangq0327@163.com (Q.W.) 2 Department of Biochemistry and Molecular Biology, Division of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA; xu.xiaolei@mayo.edu |
| AuthorAffiliation_xml | – name: 1 Department of Cardiology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China; fyd6254@gmail.com (Y.-D.F.); lwcbss@163.com (W.L.); houjianwena@126.com (J.-W.H.); guokai0201@aliyun.com (K.G.); chenxmcorrine@outlook.com (X.-M.C.); cyh1726@163.com (Y.-H.C.); wangq0327@163.com (Q.W.) – name: 2 Department of Biochemistry and Molecular Biology, Division of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA; xu.xiaolei@mayo.edu |
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| CitedBy_id | crossref_primary_10_3390_cimb45070380 crossref_primary_10_1016_j_cpcardiol_2020_100649 crossref_primary_10_1111_bph_14490 crossref_primary_10_3389_fcell_2022_826204 crossref_primary_10_1016_j_hrthm_2020_07_036 crossref_primary_10_1016_j_isci_2024_110888 crossref_primary_10_3748_wjg_v28_i48_6909 |
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| Keywords | triggered activity afterdepolarization arrhythmia oxidative stress protein kinase C |
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| SubjectTerms | Animals Cells, Cultured Kinases Membrane Potentials Myocytes, Cardiac - metabolism Myocytes, Cardiac - physiology Oxidative Stress Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism Protein Kinase Inhibitors - pharmacology Proteins Rabbits Signal Transduction |
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