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(Circulation Research. 2001;89:265.)
© 2001 American Heart Association, Inc.

Integrative Physiology

Gene Expression and In Situ Localization of Diacylglycerol Kinase Isozymes in Normal and Infarcted Rat Hearts

Effects of Captopril Treatment

Morihiko Takeda, Yutaka Kagaya, Jun Takahashi, Tadashi Sugie, Jun Ohta, Jun Watanabe, Kunio Shirato, Hisatake Kondo, Kaoru Goto

From the Department of Cardiovascular Medicine (M.T., Y.K., J.T., T.S., J.O., J.W., K.S.), Tohoku University Graduate School of Medicine, Sendai; Department of Cell Biology (H.K.), Division of Histology, Tohoku University School of Medicine, Sendai; and Department of Anatomy and Cell Biology (K.G.), Yamagata University School of Medicine, Yamagata, Japan.

Correspondence to Kaoru Goto, MD, PhD, Department of Anatomy and Cell Biology, Yamagata University School of Medicine, Iida-Nishi 2-2-2, Yamagata 990-9585, Japan. E-mail kgoto{at}med.id.yamagata-u.ac.jp

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, DGK, DGK, and DGK mRNAs were expressed evenly throughout the myocardium, although the DGK expression was very low. In infarcted hearts, the expression of DGK 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 DGK expression in the infarcted and border areas could be attributed to granulocytes and macrophages. In contrast, the expression of DGK in the infarcted and border areas was lower than that in the viable left ventricle (LV) throughout the postoperation period. Furthermore, DGK 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.

Key Words: diacylglycerol kinase • myocardial infarction • phagocytes • ventricular remodeling • angiotensin converting enzyme inhibitor

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