Key result
In human failing hearts affected by chronic volume overload, the mRNA expression of DGKη was significantly increased (P<0.0001) and DGKζ was significantly decreased (P=0.002) compared to normal hearts.
Observational (n=17)
No
This study provides the first evidence of differential regulation of DGK isoforms in human failing hearts, suggesting individual isoforms may have distinct functions in cardiac hypertrophy and heart failure.
Differential DGK isoform expression in failing hearts is hypothesis-generating; leaves open distinct functional roles and therapeutic relevance.
Evidence from several studies indicates the importance of Gαq protein-coupled receptor (GPCR) signaling pathway, which includes diacylglycerol (DAG), and protein kinase C, in the development of heart failure. DAG kinase (DGK) acts as an endogenous regulator of GPCR signaling pathway by catalyzing and regulating DAG. Expressions of DGK isoforms α, ε, and ζ in rodent hearts have been detected; however, the expression and alteration of DGK isoforms in a failing human heart has not yet been examined. In this study, we detected mRNA expressions of DGK isoforms γ, η, ε, and ζ in failing human heart samples obtained from patients undergoing cardiovascular surgery with cardiopulmonary bypass. Furthermore, we investigated modulation of DGK isoform expression in these hearts. We found that expressions of DGKη and DGKζ were increased and decreased, respectively, whereas those of DGKγ and DGKε remained unchanged. This is the first report that describes the differential regulation of DGK isoforms in normal and failing human hearts.
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Bilim et al. (2011) conducted an observational in Heart failure (n=17). Heart failure due to chronic volume overload vs. Normal heart function was evaluated on mRNA expression levels of DGK isoforms (η and ζ) (p=<0.0001). In human failing hearts affected by chronic volume overload, the mRNA expression of DGKη was significantly increased (P<0.0001) and DGKζ was significantly decreased (P=0.002) compared to normal hearts.
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