Biochemical and Biophysical Research Communications 1999-12-20

Hypernuclear acetylation in atherosclerotic lesions and activated vascular smooth muscle cells.

K Kawahara, S Watanabe, T Ohshima, Y Soejima, T Oishi, S Aratani, M Nakata, M Shibata, K Inoue, T Amano, R Fujii, K Yanai, M Hagiwara, A Fukamizu, I Maruyama, T Nakajima

Index: Biochem. Biophys. Res. Commun. 266(2) , 417-24, (1999)

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Abstract

Recent studies have implicated acetylation of several nuclear proteins such as histones and p53 on their epsilon-portion of lysine residues in eukaryotic transcription. Here we raised a specific polyclonal antibody against epsilon-acetylated lysine. Using the antibody, we detected hypernuclear acetylation (HNA) in atherosclerotic vascular smooth muscle cells (VSMCs). Thrombin, a humoral factor known to cause activation and proliferation of VSMCs, strongly potentiated HNA in cultured VSMCs. MAP kinase pathway and a signal coactivator CREB binding protein (CBP) were involved in thrombin-induced HNA of VSMCs. Our results suggest that coactivators cooperating with signal-dependent transcription activators play an important role in atherosclerogenesis via HNA in VSMCs.Copyright 1999 Academic Press.