Key result
End-stage human cardiomyopathy was associated with an almost four-fold decrease in junD mRNA levels compared to controls, while c-jun levels remained unchanged.
Observational (n=23)
In end-stage human cardiomyopathy, junD expression is significantly down-regulated while c-jun expression remains unchanged, suggesting differential regulation of these transcription factors in heart failure.
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junD downregulation may mark end-stage cardiomyopathy severity; leaves open causal role and therapeutic targeting in heart failure.
The proto-oncogenes c-jun and junD are closely related transcriptional factors with opposing actions on cell growth and division. Expression of c-jun rapidly increases as cells enter the cell cycle. Levels of c-jun are also increased in the early stages of experimental cardiac hypertrophy and failure but expression decreases with time. In contrast, junD accumulates in quiescent cells. Expression in end-stage cardiomyopathy has not been studied. Steady-state levels of c-jun and junD mRNA were determined in failing human myocardium (obtained at the time of cardiac transplantation) and in control myocardium from patients who died of noncardiac causes. Relative expression was normalized for glyceraldehyde-3-phosphate dehydrogenase expression. Levels of junD were almost four-fold depressed in myocardium from myopathic hearts (2.1 +/- 0.27, x +/- SE; n = 20) vs. the controls (7.7 +/- 1.1; n = 3). Levels of c-jun were similar in both myopathic and control hearts. Relative expression of beta-myosin heavy chain was the same in both myopathic and control hearts. Levels of junD were still found to be depressed in the myopathic hearts after normalization for myosin heavy chain gene expression. We conclude that c-jun and junD are differentially regulated in end-stage human cardiomyopathy with expression of junD being decreased while relative levels of c-jun mRNA remain unchanged. Further studies are needed to determine the role of junD down-regulation in the development and/or maintenance of the abnormalities present in end-stage heart disease.
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Pollack et al. (1997) conducted an observational in End-stage human cardiomyopathy (n=23). End-stage cardiomyopathy vs. Control myocardium from patients who died of noncardiac causes was evaluated on Steady-state levels of junD mRNA normalized for glyceraldehyde-3-phosphate dehydrogenase expression. End-stage human cardiomyopathy was associated with an almost four-fold decrease in junD mRNA levels compared to controls, while c-jun levels remained unchanged.
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