title: Gene expression and in situ localization of diacylglycerol kinase isozymes in normal and infarcted rat hearts: effects of captopril treatment.
abstract: Diacylglycerol (DG) kinase (DGK) terminates signaling from DG, which serves as an activator of protein kinase C (PKC), by converting DG to phosphatidic acid. DGK is thus regarded as an attenuator of the PKC activity. In rats, five DGK isozymes have been cloned, but little is known about their role in the heart. In this study, the spatiotemporal expression of DGK isozymes was investigated in rat hearts under a normal condition and after myocardial infarction (MI) by in situ hybridization histochemistry and immunohistochemistry. In normal left ventricular myocardium, DGKalpha, DGKepsilon, and DGKzeta mRNAs were expressed evenly throughout the myocardium, although the DGKalpha expression was very low. In infarcted hearts, the expression of DGKzeta was enhanced in the peripheral zone of the necrotic area and at the border zone 3 and 7 days after MI, and to a lesser extent in the middle layer of the granulation tissue 21 days after MI. The enhanced DGKzeta expression in the infarcted and border areas could be attributed to granulocytes and macrophages. In contrast, the expression of DGKepsilon in the infarcted and border areas was lower than that in the viable left ventricle (LV) throughout the postoperation period. Furthermore, DGKepsilon expression in the viable myocardium 21 days after MI decreased significantly compared with left ventricular myocardium in the sham-operated rats and was completely restored by treatment with captopril. Our results demonstrate that three DGK isozymes are expressed in the heart and that each isozyme might have different functional characteristics in the healing and LV remodeling after MI.
authors.affiliation: Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai.
authors.forename: M
authors.initials: M
authors.lastname: Takeda
authors.forename: Y
authors.initials: Y
authors.lastname: Kagaya
authors.forename: J
authors.initials: J
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Sugie
authors.forename: J
authors.initials: J
authors.lastname: Ohta
authors.forename: J
authors.initials: J
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Shirato
authors.forename: H
authors.initials: H
authors.lastname: Kondo
authors.forename: K
authors.initials: K
authors.lastname: Goto
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D015152:Blotting, Northern; D001835:Body Weight / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D019852:Diacylglycerol Kinase / Q000096:biosynthesis* / Q000235:genetics; D004195:Disease Models, Animal; D015870:Gene Expression / Q000187:drug effects*; D006098:Granulocytes / Q000201:enzymology; D006352:Heart Ventricles / Q000201:enzymology / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007527:Isoenzymes / Q000096:biosynthesis / Q000235:genetics; D008264:Macrophages / Q000201:enzymology; D008297:Male; D009203:Myocardial Infarction / Q000201:enzymology* / Q000473:pathology; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007527:Isoenzymes; D012333:RNA, Messenger; D002216:Captopril; D019852:Diacylglycerol Kinase