Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte Autophagy
BACKGROUND—Reperfusion accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease. Yet, no standard therapies are available targeting reperfusion injury. Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibito...
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| Published in | Circulation (New York, N.Y.) Vol. 129; no. 10; pp. 1139 - 1151 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
by the American College of Cardiology Foundation and the American Heart Association, Inc
11.03.2014
Lippincott Williams & Wilkins |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/CIRCULATIONAHA.113.002416 |
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| Abstract | BACKGROUND—Reperfusion accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease. Yet, no standard therapies are available targeting reperfusion injury. Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for cancer treatment by the US Food and Drug Administration, will blunt reperfusion injury.
METHODS AND RESULTS—Twenty-one rabbits were randomly assigned to 3 groups(1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only. Each arm was subjected to ischemia/reperfusion surgery (30 minutes coronary ligation, 24 hours reperfusion). In addition, cultured neonatal and adult rat ventricular cardiomyocytes were subjected to simulated ischemia/reperfusion to probe mechanism. SAHA reduced infarct size and partially rescued systolic function when administered either before surgery (pretreatment) or solely at the time of reperfusion. SAHA plasma concentrations were similar to those achieved in patients with cancer. In the infarct border zone, SAHA increased autophagic flux, assayed in both rabbit myocardium and in mice harboring an RFP-GFP-LC3 transgene. In cultured myocytes subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%. This reduction in cell death correlated with increased autophagic activity in SAHA-treated cells. RNAi-mediated knockdown of ATG7 and ATG5, essential autophagy proteins, abolished SAHA’s cardioprotective effects.
CONCLUSIONS—The US Food and Drug Administration–approved anticancer histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even when delivered in the clinically relevant context of reperfusion. The cardioprotective effects of SAHA during ischemia/reperfusion occur, at least in part, through the induction of autophagic flux. |
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| AbstractList | Reperfusion accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease. Yet, no standard therapies are available targeting reperfusion injury. Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for cancer treatment by the US Food and Drug Administration, will blunt reperfusion injury.
Twenty-one rabbits were randomly assigned to 3 groups: (1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only. Each arm was subjected to ischemia/reperfusion surgery (30 minutes coronary ligation, 24 hours reperfusion). In addition, cultured neonatal and adult rat ventricular cardiomyocytes were subjected to simulated ischemia/reperfusion to probe mechanism. SAHA reduced infarct size and partially rescued systolic function when administered either before surgery (pretreatment) or solely at the time of reperfusion. SAHA plasma concentrations were similar to those achieved in patients with cancer. In the infarct border zone, SAHA increased autophagic flux, assayed in both rabbit myocardium and in mice harboring an RFP-GFP-LC3 transgene. In cultured myocytes subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%. This reduction in cell death correlated with increased autophagic activity in SAHA-treated cells. RNAi-mediated knockdown of ATG7 and ATG5, essential autophagy proteins, abolished SAHA's cardioprotective effects.
The US Food and Drug Administration-approved anticancer histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even when delivered in the clinically relevant context of reperfusion. The cardioprotective effects of SAHA during ischemia/reperfusion occur, at least in part, through the induction of autophagic flux. BACKGROUND—Reperfusion accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease. Yet, no standard therapies are available targeting reperfusion injury. Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for cancer treatment by the US Food and Drug Administration, will blunt reperfusion injury. METHODS AND RESULTS—Twenty-one rabbits were randomly assigned to 3 groups(1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only. Each arm was subjected to ischemia/reperfusion surgery (30 minutes coronary ligation, 24 hours reperfusion). In addition, cultured neonatal and adult rat ventricular cardiomyocytes were subjected to simulated ischemia/reperfusion to probe mechanism. SAHA reduced infarct size and partially rescued systolic function when administered either before surgery (pretreatment) or solely at the time of reperfusion. SAHA plasma concentrations were similar to those achieved in patients with cancer. In the infarct border zone, SAHA increased autophagic flux, assayed in both rabbit myocardium and in mice harboring an RFP-GFP-LC3 transgene. In cultured myocytes subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%. This reduction in cell death correlated with increased autophagic activity in SAHA-treated cells. RNAi-mediated knockdown of ATG7 and ATG5, essential autophagy proteins, abolished SAHA’s cardioprotective effects. CONCLUSIONS—The US Food and Drug Administration–approved anticancer histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even when delivered in the clinically relevant context of reperfusion. The cardioprotective effects of SAHA during ischemia/reperfusion occur, at least in part, through the induction of autophagic flux. Reperfusion accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease. Yet, no standard therapies are available targeting reperfusion injury. Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for cancer treatment by the US Food and Drug Administration, will blunt reperfusion injury.BACKGROUNDReperfusion accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease. Yet, no standard therapies are available targeting reperfusion injury. Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for cancer treatment by the US Food and Drug Administration, will blunt reperfusion injury.Twenty-one rabbits were randomly assigned to 3 groups: (1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only. Each arm was subjected to ischemia/reperfusion surgery (30 minutes coronary ligation, 24 hours reperfusion). In addition, cultured neonatal and adult rat ventricular cardiomyocytes were subjected to simulated ischemia/reperfusion to probe mechanism. SAHA reduced infarct size and partially rescued systolic function when administered either before surgery (pretreatment) or solely at the time of reperfusion. SAHA plasma concentrations were similar to those achieved in patients with cancer. In the infarct border zone, SAHA increased autophagic flux, assayed in both rabbit myocardium and in mice harboring an RFP-GFP-LC3 transgene. In cultured myocytes subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%. This reduction in cell death correlated with increased autophagic activity in SAHA-treated cells. RNAi-mediated knockdown of ATG7 and ATG5, essential autophagy proteins, abolished SAHA's cardioprotective effects.METHODS AND RESULTSTwenty-one rabbits were randomly assigned to 3 groups: (1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only. Each arm was subjected to ischemia/reperfusion surgery (30 minutes coronary ligation, 24 hours reperfusion). In addition, cultured neonatal and adult rat ventricular cardiomyocytes were subjected to simulated ischemia/reperfusion to probe mechanism. SAHA reduced infarct size and partially rescued systolic function when administered either before surgery (pretreatment) or solely at the time of reperfusion. SAHA plasma concentrations were similar to those achieved in patients with cancer. In the infarct border zone, SAHA increased autophagic flux, assayed in both rabbit myocardium and in mice harboring an RFP-GFP-LC3 transgene. In cultured myocytes subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%. This reduction in cell death correlated with increased autophagic activity in SAHA-treated cells. RNAi-mediated knockdown of ATG7 and ATG5, essential autophagy proteins, abolished SAHA's cardioprotective effects.The US Food and Drug Administration-approved anticancer histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even when delivered in the clinically relevant context of reperfusion. The cardioprotective effects of SAHA during ischemia/reperfusion occur, at least in part, through the induction of autophagic flux.CONCLUSIONSThe US Food and Drug Administration-approved anticancer histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even when delivered in the clinically relevant context of reperfusion. The cardioprotective effects of SAHA during ischemia/reperfusion occur, at least in part, through the induction of autophagic flux. |
| Author | Xie, Min Lavandero, Sergio Morales, Cyndi Luo, Xiang Hill, Joseph A. Pedrozo, Zully Jessen, Michael E. Wang, Zhao V. Jiang, Nan Kong, Yongli May, Herman Warner, John J. Battiprolu, Pavan K. Tan, Wei Gillette, Thomas G. Turer, Aslan T. Cho, Geoffrey |
| AuthorAffiliation | From the Departments of Internal Medicine (Cardiology) (M.X., Y.K., W.Y., H.M., P.K.B., Z.P., Z.V.W., C.M., X.L., G.C., N.J., J.J.W., S.L., T.G.G., A.T.T., J.A.H.), Cardiovascular and Thoracic Surgery (M.E.J.), Advanced Center for Chronic Diseases (ACCDiS) & Centro Estudios Moleculares de la Celula, Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile (S.L.); and the Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas (J.A.H.) |
| AuthorAffiliation_xml | – name: From the Departments of Internal Medicine (Cardiology) (M.X., Y.K., W.Y., H.M., P.K.B., Z.P., Z.V.W., C.M., X.L., G.C., N.J., J.J.W., S.L., T.G.G., A.T.T., J.A.H.), Cardiovascular and Thoracic Surgery (M.E.J.), Advanced Center for Chronic Diseases (ACCDiS) & Centro Estudios Moleculares de la Celula, Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile (S.L.); and the Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas (J.A.H.) |
| Author_xml | – sequence: 1 givenname: Min surname: Xie fullname: Xie, Min organization: From the Departments of Internal Medicine (Cardiology) (M.X., Y.K., W.Y., H.M., P.K.B., Z.P., Z.V.W., C.M., X.L., G.C., N.J., J.J.W., S.L., T.G.G., A.T.T., J.A.H.), Cardiovascular and Thoracic Surgery (M.E.J.), Advanced Center for Chronic Diseases (ACCDiS) & Centro Estudios Moleculares de la Celula, Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile (S.L.); and the Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas (J.A.H.) – sequence: 2 givenname: Yongli surname: Kong fullname: Kong, Yongli – sequence: 3 givenname: Wei surname: Tan fullname: Tan, Wei – sequence: 4 givenname: Herman surname: May fullname: May, Herman – sequence: 5 givenname: Pavan surname: Battiprolu middlename: K. fullname: Battiprolu, Pavan K. – sequence: 6 givenname: Zully surname: Pedrozo fullname: Pedrozo, Zully – sequence: 7 givenname: Zhao surname: Wang middlename: V. fullname: Wang, Zhao V. – sequence: 8 givenname: Cyndi surname: Morales fullname: Morales, Cyndi – sequence: 9 givenname: Xiang surname: Luo fullname: Luo, Xiang – sequence: 10 givenname: Geoffrey surname: Cho fullname: Cho, Geoffrey – sequence: 11 givenname: Nan surname: Jiang fullname: Jiang, Nan – sequence: 12 givenname: Michael surname: Jessen middlename: E. fullname: Jessen, Michael E. – sequence: 13 givenname: John surname: Warner middlename: J. fullname: Warner, John J. – sequence: 14 givenname: Sergio surname: Lavandero fullname: Lavandero, Sergio – sequence: 15 givenname: Thomas surname: Gillette middlename: G. fullname: Gillette, Thomas G. – sequence: 16 givenname: Aslan surname: Turer middlename: T. fullname: Turer, Aslan T. – sequence: 17 givenname: Joseph surname: Hill middlename: A. fullname: Hill, Joseph A. |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28355470$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/24396039$$D View this record in MEDLINE/PubMed |
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| Keywords | Heart Myocardial infarction autophagy Injury Cardiovascular disease reperfusion injury Coronary heart disease Myocardial disease Trauma Myocyte Reperfusion Ischemia Cell death Blunted effect histone deacetylases Circulatory system Inhibition Lesion Cardiology Histone cell death myocardial infarction |
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| SubjectTerms | Animals Animals, Genetically Modified Apoptosis - drug effects Autophagy - drug effects Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cells, Cultured Coronary heart disease Disease Models, Animal Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Heart Histone Deacetylase Inhibitors - pharmacology Histone Deacetylase Inhibitors - therapeutic use Histone Deacetylases - drug effects Humans Hydroxamic Acids - pharmacology Hydroxamic Acids - therapeutic use Male Medical sciences Mice Mice, Inbred C57BL Myocardial Infarction - pathology Myocardial Infarction - prevention & control Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control Myocarditis. Cardiomyopathies Myocytes, Cardiac - drug effects Myocytes, Cardiac - pathology Rabbits Rats Rats, Sprague-Dawley |
| Title | Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte Autophagy |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/24396039 https://www.proquest.com/docview/1506795885 |
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