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Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion
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| Zeitschriftentitel: | Circulation |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , |
| In: | Circulation, 99, 1999, 13, S. 1685-1691 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Ma, Xin L. Kumar, Sanjay Gao, Feng Louden, Calvert S. Lopez, Bernard L. Christopher, Theodore A. Wang, Chuanlin Lee, John C. Feuerstein, Giora Z. Yue, Tian-Li Ma, Xin L. Kumar, Sanjay Gao, Feng Louden, Calvert S. Lopez, Bernard L. Christopher, Theodore A. Wang, Chuanlin Lee, John C. Feuerstein, Giora Z. Yue, Tian-Li |
|---|---|
| author |
Ma, Xin L. Kumar, Sanjay Gao, Feng Louden, Calvert S. Lopez, Bernard L. Christopher, Theodore A. Wang, Chuanlin Lee, John C. Feuerstein, Giora Z. Yue, Tian-Li |
| spellingShingle |
Ma, Xin L. Kumar, Sanjay Gao, Feng Louden, Calvert S. Lopez, Bernard L. Christopher, Theodore A. Wang, Chuanlin Lee, John C. Feuerstein, Giora Z. Yue, Tian-Li Circulation Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion Physiology (medical) Cardiology and Cardiovascular Medicine |
| author_sort |
ma, xin l. |
| spelling |
Ma, Xin L. Kumar, Sanjay Gao, Feng Louden, Calvert S. Lopez, Bernard L. Christopher, Theodore A. Wang, Chuanlin Lee, John C. Feuerstein, Giora Z. Yue, Tian-Li 0009-7322 1524-4539 Ovid Technologies (Wolters Kluwer Health) Physiology (medical) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/01.cir.99.13.1685 <jats:p> <jats:italic>Background</jats:italic> —Activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in apoptotic cell death. The role of p38 MAPK in myocardial injury caused by ischemia/reperfusion, an extreme stress to the heart, is unknown. </jats:p> <jats:p> <jats:italic>Methods and Results</jats:italic> —Studies were performed with isolated, Langendorff-perfused rabbit hearts. Ischemia alone caused a moderate but transient increase in p38 MAPK activity (3.5-fold increase, <jats:italic>P</jats:italic> <0.05 versus basal). Ischemia followed by reperfusion further activated p38 MAPK, and the maximal level of activation (6.3-fold, <jats:italic>P</jats:italic> <0.01) was reached 10 minutes after reperfusion. Administration of SB 203580, a p38 MAPK inhibitor, decreased myocardial apoptosis (14.7±3.2% versus 30.6±3.5% in vehicle, <jats:italic>P</jats:italic> <0.01) and improved postischemic cardiac function. The cardioprotective effects of SB 203580 were closely related to its inhibition of p38 MAPK. Administering SB 203580 before ischemia and during reperfusion completely inhibited p38 MAPK activation and exerted the most cardioprotective effects. In contrast, administering SB 203580 10 minutes after reperfusion (a time point when maximal MAPK activation had already been achieved) failed to convey significant cardioprotection. Moreover, inhibition of p38 MAPK attenuated myocardial necrosis after a prolonged reperfusion. </jats:p> <jats:p> <jats:italic>Conclusions</jats:italic> —These results demonstrate that p38 MAPK plays a pivotal role in the signal transduction pathway mediating postischemic myocardial apoptosis and that inhibiting p38 MAPK may attenuate reperfusion injury. </jats:p> Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion Circulation |
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Medizin Biologie |
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Ovid Technologies (Wolters Kluwer Health), 1999 |
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Circulation |
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| title |
Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_unstemmed |
Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_full |
Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_fullStr |
Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_full_unstemmed |
Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_short |
Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_sort |
inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion |
| topic |
Physiology (medical) Cardiology and Cardiovascular Medicine |
| url |
http://dx.doi.org/10.1161/01.cir.99.13.1685 |
| publishDate |
1999 |
| physical |
1685-1691 |
| description |
<jats:p>
<jats:italic>Background</jats:italic>
—Activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in apoptotic cell death. The role of p38 MAPK in myocardial injury caused by ischemia/reperfusion, an extreme stress to the heart, is unknown.
</jats:p>
<jats:p>
<jats:italic>Methods and Results</jats:italic>
—Studies were performed with isolated, Langendorff-perfused rabbit hearts. Ischemia alone caused a moderate but transient increase in p38 MAPK activity (3.5-fold increase,
<jats:italic>P</jats:italic>
<0.05 versus basal). Ischemia followed by reperfusion further activated p38 MAPK, and the maximal level of activation (6.3-fold,
<jats:italic>P</jats:italic>
<0.01) was reached 10 minutes after reperfusion. Administration of SB 203580, a p38 MAPK inhibitor, decreased myocardial apoptosis (14.7±3.2% versus 30.6±3.5% in vehicle,
<jats:italic>P</jats:italic>
<0.01) and improved postischemic cardiac function. The cardioprotective effects of SB 203580 were closely related to its inhibition of p38 MAPK. Administering SB 203580 before ischemia and during reperfusion completely inhibited p38 MAPK activation and exerted the most cardioprotective effects. In contrast, administering SB 203580 10 minutes after reperfusion (a time point when maximal MAPK activation had already been achieved) failed to convey significant cardioprotection. Moreover, inhibition of p38 MAPK attenuated myocardial necrosis after a prolonged reperfusion.
</jats:p>
<jats:p>
<jats:italic>Conclusions</jats:italic>
—These results demonstrate that p38 MAPK plays a pivotal role in the signal transduction pathway mediating postischemic myocardial apoptosis and that inhibiting p38 MAPK may attenuate reperfusion injury.
</jats:p> |
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| author | Ma, Xin L., Kumar, Sanjay, Gao, Feng, Louden, Calvert S., Lopez, Bernard L., Christopher, Theodore A., Wang, Chuanlin, Lee, John C., Feuerstein, Giora Z., Yue, Tian-Li |
| author_facet | Ma, Xin L., Kumar, Sanjay, Gao, Feng, Louden, Calvert S., Lopez, Bernard L., Christopher, Theodore A., Wang, Chuanlin, Lee, John C., Feuerstein, Giora Z., Yue, Tian-Li, Ma, Xin L., Kumar, Sanjay, Gao, Feng, Louden, Calvert S., Lopez, Bernard L., Christopher, Theodore A., Wang, Chuanlin, Lee, John C., Feuerstein, Giora Z., Yue, Tian-Li |
| author_sort | ma, xin l. |
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| description | <jats:p> <jats:italic>Background</jats:italic> —Activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in apoptotic cell death. The role of p38 MAPK in myocardial injury caused by ischemia/reperfusion, an extreme stress to the heart, is unknown. </jats:p> <jats:p> <jats:italic>Methods and Results</jats:italic> —Studies were performed with isolated, Langendorff-perfused rabbit hearts. Ischemia alone caused a moderate but transient increase in p38 MAPK activity (3.5-fold increase, <jats:italic>P</jats:italic> <0.05 versus basal). Ischemia followed by reperfusion further activated p38 MAPK, and the maximal level of activation (6.3-fold, <jats:italic>P</jats:italic> <0.01) was reached 10 minutes after reperfusion. Administration of SB 203580, a p38 MAPK inhibitor, decreased myocardial apoptosis (14.7±3.2% versus 30.6±3.5% in vehicle, <jats:italic>P</jats:italic> <0.01) and improved postischemic cardiac function. The cardioprotective effects of SB 203580 were closely related to its inhibition of p38 MAPK. Administering SB 203580 before ischemia and during reperfusion completely inhibited p38 MAPK activation and exerted the most cardioprotective effects. In contrast, administering SB 203580 10 minutes after reperfusion (a time point when maximal MAPK activation had already been achieved) failed to convey significant cardioprotection. Moreover, inhibition of p38 MAPK attenuated myocardial necrosis after a prolonged reperfusion. </jats:p> <jats:p> <jats:italic>Conclusions</jats:italic> —These results demonstrate that p38 MAPK plays a pivotal role in the signal transduction pathway mediating postischemic myocardial apoptosis and that inhibiting p38 MAPK may attenuate reperfusion injury. </jats:p> |
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| imprint | Ovid Technologies (Wolters Kluwer Health), 1999 |
| imprint_str_mv | Ovid Technologies (Wolters Kluwer Health), 1999 |
| institution | DE-Zwi2, DE-D161, DE-Zi4, DE-Gla1, DE-15, DE-Pl11, DE-Rs1, DE-14, DE-105, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1 |
| issn | 0009-7322, 1524-4539 |
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| mega_collection | Ovid Technologies (Wolters Kluwer Health) (CrossRef) |
| physical | 1685-1691 |
| publishDate | 1999 |
| publishDateSort | 1999 |
| publisher | Ovid Technologies (Wolters Kluwer Health) |
| record_format | ai |
| recordtype | ai |
| series | Circulation |
| source_id | 49 |
| spelling | Ma, Xin L. Kumar, Sanjay Gao, Feng Louden, Calvert S. Lopez, Bernard L. Christopher, Theodore A. Wang, Chuanlin Lee, John C. Feuerstein, Giora Z. Yue, Tian-Li 0009-7322 1524-4539 Ovid Technologies (Wolters Kluwer Health) Physiology (medical) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/01.cir.99.13.1685 <jats:p> <jats:italic>Background</jats:italic> —Activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in apoptotic cell death. The role of p38 MAPK in myocardial injury caused by ischemia/reperfusion, an extreme stress to the heart, is unknown. </jats:p> <jats:p> <jats:italic>Methods and Results</jats:italic> —Studies were performed with isolated, Langendorff-perfused rabbit hearts. Ischemia alone caused a moderate but transient increase in p38 MAPK activity (3.5-fold increase, <jats:italic>P</jats:italic> <0.05 versus basal). Ischemia followed by reperfusion further activated p38 MAPK, and the maximal level of activation (6.3-fold, <jats:italic>P</jats:italic> <0.01) was reached 10 minutes after reperfusion. Administration of SB 203580, a p38 MAPK inhibitor, decreased myocardial apoptosis (14.7±3.2% versus 30.6±3.5% in vehicle, <jats:italic>P</jats:italic> <0.01) and improved postischemic cardiac function. The cardioprotective effects of SB 203580 were closely related to its inhibition of p38 MAPK. Administering SB 203580 before ischemia and during reperfusion completely inhibited p38 MAPK activation and exerted the most cardioprotective effects. In contrast, administering SB 203580 10 minutes after reperfusion (a time point when maximal MAPK activation had already been achieved) failed to convey significant cardioprotection. Moreover, inhibition of p38 MAPK attenuated myocardial necrosis after a prolonged reperfusion. </jats:p> <jats:p> <jats:italic>Conclusions</jats:italic> —These results demonstrate that p38 MAPK plays a pivotal role in the signal transduction pathway mediating postischemic myocardial apoptosis and that inhibiting p38 MAPK may attenuate reperfusion injury. </jats:p> Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion Circulation |
| spellingShingle | Ma, Xin L., Kumar, Sanjay, Gao, Feng, Louden, Calvert S., Lopez, Bernard L., Christopher, Theodore A., Wang, Chuanlin, Lee, John C., Feuerstein, Giora Z., Yue, Tian-Li, Circulation, Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion, Physiology (medical), Cardiology and Cardiovascular Medicine |
| title | Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_full | Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_fullStr | Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_full_unstemmed | Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_short | Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| title_sort | inhibition of p38 mitogen-activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion |
| title_unstemmed | Inhibition of p38 Mitogen-Activated Protein Kinase Decreases Cardiomyocyte Apoptosis and Improves Cardiac Function After Myocardial Ischemia and Reperfusion |
| topic | Physiology (medical), Cardiology and Cardiovascular Medicine |
| url | http://dx.doi.org/10.1161/01.cir.99.13.1685 |