NDLI: Terminal Deoxynucleotidyl Transferase – Mediated dUTP Nick-End-Labeling Assays

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Terminal Deoxynucleotidyl Transferase – Mediated dUTP Nick-End-Labeling Assays

Content Provider	Semantic Scholar
Author	Zhao, Xiao-Song Pan, Wentong Bekeredjian, Raffi Shohet, Ralph V.
Copyright Year	2006
Abstract	Background—Endothelin-1 (ET-1) has potent vasoconstrictor and hypertrophic actions. Pharmacological antagonists of endothelin receptors attenuate cardiac hypertrophy, have been approved for treatment of pulmonary hypertension, and are under investigation for treatment of heart failure. To investigate the role of ET-1 in the heart, we created mice with cardiomyocyte deletion of ET-1. Methods and Results—Mice with cardiomyocyte-specific deletion of ET-1 are phenotypically normal when young. Remarkably, as the mice age or when young animals are subjected to aortic banding, they develop an unexpected phenotype of progressive systolic dysfunction and cardiac dilation. Echocardiography, necropsy, histology, and molecular phenotype confirm a dilated cardiomyopathy. Terminal deoxynucleotidyl transferase–mediated dUTP nick-end-labeling analysis reveals greater abundance of apoptotic nuclei in the ET-1–deficient hearts. Transcriptional and Western analyses suggest enhanced tumor necrosis factor (TNF)–mediated apoptosis with increases in caspase-8 activity. These ET-1–deficient hearts also have diminished nuclear factor (NF)B activity, resulting in diminution of downstream inhibitors of TNF signaling. Conclusions—Local ET-1 gene expression is necessary to maintain normal cardiac function and cardiomyocyte survival in mice with both age and hemodynamic stress. This cardiac-protective effect is mediated by paracrine ET-1 modulation of TNF-related apoptosis, in part through upregulation of NFB signaling. (Circulation. 2006;114:830-837.)
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://circ.ahajournals.org/content/circulationaha/114/8/830.full.pdf?download=true
Alternate Webpage(s)	http://circ.ahajournals.org/content/circulationaha/114/8/830.full.pdf
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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