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Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury
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| Zeitschriftentitel: | Circulation Research |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | Circulation Research, 111, 2012, suppl_1 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Xu, Zhaobin Wheeler, Debra G Mahamud, Shouvik D Dwyer, Karen M Robson, Simon C Cowan, Peter J d'Apice, Anthony J Gumina, Richard J Xu, Zhaobin Wheeler, Debra G Mahamud, Shouvik D Dwyer, Karen M Robson, Simon C Cowan, Peter J d'Apice, Anthony J Gumina, Richard J |
|---|---|
| author |
Xu, Zhaobin Wheeler, Debra G Mahamud, Shouvik D Dwyer, Karen M Robson, Simon C Cowan, Peter J d'Apice, Anthony J Gumina, Richard J |
| spellingShingle |
Xu, Zhaobin Wheeler, Debra G Mahamud, Shouvik D Dwyer, Karen M Robson, Simon C Cowan, Peter J d'Apice, Anthony J Gumina, Richard J Circulation Research Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury Cardiology and Cardiovascular Medicine Physiology |
| author_sort |
xu, zhaobin |
| spelling |
Xu, Zhaobin Wheeler, Debra G Mahamud, Shouvik D Dwyer, Karen M Robson, Simon C Cowan, Peter J d'Apice, Anthony J Gumina, Richard J 0009-7330 1524-4571 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1161/res.111.suppl_1.a289 <jats:p> <jats:bold>Background:</jats:bold> During myocardial stress, extracellular levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) increase. These extracellular ATP and ADP levels are modulated via hydrolysis by ectonucleoside triphosphate diphosphohydrolase 1 (ENTDP-1/CD39) to adenosine monophosphate (AMP) subsequently converted by ecto-5'-nucleotidase (CD73) to the anti-thrombotic, cardioprotective nucleoside, adenosine. Previous data demonstrated significantly smaller infarcts in mice globally overexpressing CD39. The current objective was to determine whether tissue specific overexpression of CD39 in the heart would reduce myocardial ischemia/reperfusion injury. </jats:p> <jats:p> <jats:bold>Methods:</jats:bold> Myocardial ischemia/reperfusion (I/R) injury was evaluated in transgenic mice overexpressing human CD39 driven by the α-MHC promoter. I/R injury was induced by ligation of the left anterior descending (LAD) artery for 60 min followed by 24 hours of reperfusion. Myocardial infarct size was determined by staining with triphenyl tetrazolium chloride (TTC) and the area-at-risk was delineated by perfusion with 5% Phthalo Blue. </jats:p> <jats:p> <jats:bold>Results:</jats:bold> Expression of CD39 in the heart tissue was confirmed by Western blot analysis. In response to 60 minutes of ischemia followed by 24 hours of reperfusion, α-MHC CD39-OE animals displayed a marked reduction in infarct size (WT: 31.68%±4.64 vs TG: 6.14%± 2.48, N=5/group, P<0.01), relative to wild-type controls (Figure). </jats:p> <jats:p> <jats:bold>Conclusions:</jats:bold> Overexpression of CD39 in cardiac tissue alone significantly attenuates myocardial ischemic injury. </jats:p> <jats:p> <jats:fig orientation="portrait" position="anchor"> <jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" orientation="portrait" position="float" xlink:href="g499_1.jpeg" /> </jats:fig> </jats:p> Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury Circulation Research |
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Ovid Technologies (Wolters Kluwer Health), 2012 |
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Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_unstemmed |
Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_full |
Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_fullStr |
Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_full_unstemmed |
Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_short |
Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_sort |
abstract 289: cardiac-specific ectonucleoside triphosphate diphosphohydrolase 1 overexpression affords protection from myocardial infarction and reperfusion injury |
| topic |
Cardiology and Cardiovascular Medicine Physiology |
| url |
http://dx.doi.org/10.1161/res.111.suppl_1.a289 |
| publishDate |
2012 |
| physical |
|
| description |
<jats:p>
<jats:bold>Background:</jats:bold>
During myocardial stress, extracellular levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) increase. These extracellular ATP and ADP levels are modulated via hydrolysis by ectonucleoside triphosphate diphosphohydrolase 1 (ENTDP-1/CD39) to adenosine monophosphate (AMP) subsequently converted by ecto-5'-nucleotidase (CD73) to the anti-thrombotic, cardioprotective nucleoside, adenosine. Previous data demonstrated significantly smaller infarcts in mice globally overexpressing CD39. The current objective was to determine whether tissue specific overexpression of CD39 in the heart would reduce myocardial ischemia/reperfusion injury.
</jats:p>
<jats:p>
<jats:bold>Methods:</jats:bold>
Myocardial ischemia/reperfusion (I/R) injury was evaluated in transgenic mice overexpressing human CD39 driven by the α-MHC promoter. I/R injury was induced by ligation of the left anterior descending (LAD) artery for 60 min followed by 24 hours of reperfusion. Myocardial infarct size was determined by staining with triphenyl tetrazolium chloride (TTC) and the area-at-risk was delineated by perfusion with 5% Phthalo Blue.
</jats:p>
<jats:p>
<jats:bold>Results:</jats:bold>
Expression of CD39 in the heart tissue was confirmed by Western blot analysis. In response to 60 minutes of ischemia followed by 24 hours of reperfusion, α-MHC CD39-OE animals displayed a marked reduction in infarct size (WT: 31.68%±4.64 vs TG: 6.14%± 2.48, N=5/group, P<0.01), relative to wild-type controls (Figure).
</jats:p>
<jats:p>
<jats:bold>Conclusions:</jats:bold>
Overexpression of CD39 in cardiac tissue alone significantly attenuates myocardial ischemic injury.
</jats:p>
<jats:p>
<jats:fig orientation="portrait" position="anchor">
<jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" orientation="portrait" position="float" xlink:href="g499_1.jpeg" />
</jats:fig>
</jats:p> |
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| author | Xu, Zhaobin, Wheeler, Debra G, Mahamud, Shouvik D, Dwyer, Karen M, Robson, Simon C, Cowan, Peter J, d'Apice, Anthony J, Gumina, Richard J |
| author_facet | Xu, Zhaobin, Wheeler, Debra G, Mahamud, Shouvik D, Dwyer, Karen M, Robson, Simon C, Cowan, Peter J, d'Apice, Anthony J, Gumina, Richard J, Xu, Zhaobin, Wheeler, Debra G, Mahamud, Shouvik D, Dwyer, Karen M, Robson, Simon C, Cowan, Peter J, d'Apice, Anthony J, Gumina, Richard J |
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| description | <jats:p> <jats:bold>Background:</jats:bold> During myocardial stress, extracellular levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) increase. These extracellular ATP and ADP levels are modulated via hydrolysis by ectonucleoside triphosphate diphosphohydrolase 1 (ENTDP-1/CD39) to adenosine monophosphate (AMP) subsequently converted by ecto-5'-nucleotidase (CD73) to the anti-thrombotic, cardioprotective nucleoside, adenosine. Previous data demonstrated significantly smaller infarcts in mice globally overexpressing CD39. The current objective was to determine whether tissue specific overexpression of CD39 in the heart would reduce myocardial ischemia/reperfusion injury. </jats:p> <jats:p> <jats:bold>Methods:</jats:bold> Myocardial ischemia/reperfusion (I/R) injury was evaluated in transgenic mice overexpressing human CD39 driven by the α-MHC promoter. I/R injury was induced by ligation of the left anterior descending (LAD) artery for 60 min followed by 24 hours of reperfusion. Myocardial infarct size was determined by staining with triphenyl tetrazolium chloride (TTC) and the area-at-risk was delineated by perfusion with 5% Phthalo Blue. </jats:p> <jats:p> <jats:bold>Results:</jats:bold> Expression of CD39 in the heart tissue was confirmed by Western blot analysis. In response to 60 minutes of ischemia followed by 24 hours of reperfusion, α-MHC CD39-OE animals displayed a marked reduction in infarct size (WT: 31.68%±4.64 vs TG: 6.14%± 2.48, N=5/group, P<0.01), relative to wild-type controls (Figure). </jats:p> <jats:p> <jats:bold>Conclusions:</jats:bold> Overexpression of CD39 in cardiac tissue alone significantly attenuates myocardial ischemic injury. </jats:p> <jats:p> <jats:fig orientation="portrait" position="anchor"> <jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" orientation="portrait" position="float" xlink:href="g499_1.jpeg" /> </jats:fig> </jats:p> |
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| imprint | Ovid Technologies (Wolters Kluwer Health), 2012 |
| imprint_str_mv | Ovid Technologies (Wolters Kluwer Health), 2012 |
| institution | DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4 |
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| spelling | Xu, Zhaobin Wheeler, Debra G Mahamud, Shouvik D Dwyer, Karen M Robson, Simon C Cowan, Peter J d'Apice, Anthony J Gumina, Richard J 0009-7330 1524-4571 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1161/res.111.suppl_1.a289 <jats:p> <jats:bold>Background:</jats:bold> During myocardial stress, extracellular levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) increase. These extracellular ATP and ADP levels are modulated via hydrolysis by ectonucleoside triphosphate diphosphohydrolase 1 (ENTDP-1/CD39) to adenosine monophosphate (AMP) subsequently converted by ecto-5'-nucleotidase (CD73) to the anti-thrombotic, cardioprotective nucleoside, adenosine. Previous data demonstrated significantly smaller infarcts in mice globally overexpressing CD39. The current objective was to determine whether tissue specific overexpression of CD39 in the heart would reduce myocardial ischemia/reperfusion injury. </jats:p> <jats:p> <jats:bold>Methods:</jats:bold> Myocardial ischemia/reperfusion (I/R) injury was evaluated in transgenic mice overexpressing human CD39 driven by the α-MHC promoter. I/R injury was induced by ligation of the left anterior descending (LAD) artery for 60 min followed by 24 hours of reperfusion. Myocardial infarct size was determined by staining with triphenyl tetrazolium chloride (TTC) and the area-at-risk was delineated by perfusion with 5% Phthalo Blue. </jats:p> <jats:p> <jats:bold>Results:</jats:bold> Expression of CD39 in the heart tissue was confirmed by Western blot analysis. In response to 60 minutes of ischemia followed by 24 hours of reperfusion, α-MHC CD39-OE animals displayed a marked reduction in infarct size (WT: 31.68%±4.64 vs TG: 6.14%± 2.48, N=5/group, P<0.01), relative to wild-type controls (Figure). </jats:p> <jats:p> <jats:bold>Conclusions:</jats:bold> Overexpression of CD39 in cardiac tissue alone significantly attenuates myocardial ischemic injury. </jats:p> <jats:p> <jats:fig orientation="portrait" position="anchor"> <jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" orientation="portrait" position="float" xlink:href="g499_1.jpeg" /> </jats:fig> </jats:p> Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury Circulation Research |
| spellingShingle | Xu, Zhaobin, Wheeler, Debra G, Mahamud, Shouvik D, Dwyer, Karen M, Robson, Simon C, Cowan, Peter J, d'Apice, Anthony J, Gumina, Richard J, Circulation Research, Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury, Cardiology and Cardiovascular Medicine, Physiology |
| title | Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_full | Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_fullStr | Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_full_unstemmed | Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_short | Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| title_sort | abstract 289: cardiac-specific ectonucleoside triphosphate diphosphohydrolase 1 overexpression affords protection from myocardial infarction and reperfusion injury |
| title_unstemmed | Abstract 289: Cardiac-Specific Ectonucleoside Triphosphate Diphosphohydrolase 1 Overexpression Affords Protection from Myocardial Infarction and Reperfusion Injury |
| topic | Cardiology and Cardiovascular Medicine, Physiology |
| url | http://dx.doi.org/10.1161/res.111.suppl_1.a289 |