Upregulation of Phospholipase D Expression and Activation in Ventricular Pressure-Overload Hypertrophy

Upregulation of Phospholipase D Expression and Activation in Ventricular Pressure-Overload Hypertrophy

Evidence for a role of phospholipase D (PLD) in cellular proliferation and differentiation is accumulating. We studied PLD activity and expression in normal and hypertrophic rat and human hearts. In rat heart, abdominal aortic banding (constriction to 50% of original lumen) caused hypertrophy in the...

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Published in:Journal of Pharmacological Sciences Vol. 98; no. 3; pp. 244 - 254
Main Authors: Peivandi, Ali A., Huhn, Alexander, Lehr, Hans-Anton, Jin, Shenchu, Troost, Joachim, Salha, Sonia, Weismüller, Tobias, Löffelholz, Konrad
Format: Journal Article
Language:English
Published: Japan Elsevier B.V 2005
The Japanese Pharmacological Society
Elsevier
Subjects:
Animals
Blotting, Western
Body Weight
cardiac hypertrophy
Cardiomegaly - enzymology
Cardiomegaly - etiology
Enzyme Activation
Gene Expression Regulation, Enzymologic
Humans
Isoenzymes - genetics
Isoenzymes - metabolism
Male
phospholipase D
Phospholipase D - genetics
Phospholipase D - metabolism
protein kinase C
Protein Kinase C - physiology
Rats
Rats, Sprague-Dawley
Receptors, Adrenergic - physiology
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - analysis
Signal Transduction
Up-Regulation
Ventricular Pressure
α-adrenoceptor
phospholipase D
α-adrenoceptor
cardiac hypertrophy
signal transduction
protein kinase C
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Summary:Evidence for a role of phospholipase D (PLD) in cellular proliferation and differentiation is accumulating. We studied PLD activity and expression in normal and hypertrophic rat and human hearts. In rat heart, abdominal aortic banding (constriction to 50% of original lumen) caused hypertrophy in the left ventricle (as shown by weight index and ANP expression) by about 15% after 30 days without histological evidence of fibrosis or signs of decompensation and in the right ventricle after 100 days. The hypertrophy was accompanied by small increases of basal PLD activity and strong potentiation of stimulated PLD activity caused by 4β-phorbol-12β,13α-dibutyrate (PDB) and by phenylephrine. The mRNA expressions of both PLD1 and PLD2 determined by semiquantitative competitive RT-PCR were markedly enhanced after aortic banding. In the caveolar fraction of the rat heart, PLD2 protein determined by Western blot analysis was upregulated in parallel with the expression of caveolin-3. A similar induction of PLD mRNA and protein expression was observed in hypertrophied human hearts of individuals (39 – 45-year-old) who had died from non-cardiac causes. In conclusion, PLD1 and PLD2 expressions were strongly enhanced both in rat and human heart hypertrophy, which may be responsible for the coincident potentiation of the PLD activation by α-adrenoceptor and protein kinase C stimulation. These results are compatible with a significant role of PLD activation in cell signaling of ventricular pressure-overload hypertrophy.
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ISSN:1347-8613
1347-8648
DOI:10.1254/jphs.FPE04008X