Enhancement by α-tocopheryl hemisuccinate of nitric oxide production induced by lypopolysaccharide and interferon-γ through the upregulation of protein kinase C in rat vascular smooth muscle cells

被引:14
作者
Kogure, K [1 ]
Morita, M [1 ]
Hama, S [1 ]
Nakashima, S [1 ]
Tokumura, A [1 ]
Fukuzawa, K [1 ]
机构
[1] Univ Tokushima, Fac Pharmaceut Sci, Tokushima 7708505, Japan
来源
EUROPEAN JOURNAL OF BIOCHEMISTRY | 2002年 / 269卷 / 09期
关键词
alpha-tocopheryl hemisuccunate; alpha-tocopherol; nitric oxide; vascular smooth muscle cells; protein kinase C;
D O I
10.1046/j.1432-1033.2002.02894.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effect of alpha-tocopheryl hemisuccinate (TS) on lipopolysaccharide (LPS)/interferon-gamma (IFN)-induced nitric oxide production in rat vascular smooth muscle cells (VSMC) was examined. The LPS/IFN-induced NO production was enhanced by TS but not by the otheralpha-tocopherol (alpha-T) derivatives alpha-tocopheryl acetate (TA) and alpha-tocopheryl nicotinate (TN), or alpha-T itself. alpha-T, TA and TN inhibited the enhancement by TS of LPS/IFN-induced NO production. The enhancing effect of TS was observed in the presence of LPS, but not IFN, suggesting that TS participates in the LPS-stimulated signal pathway leading to NO production. Protein kinase C (PKC) inhibitors, but not protein kinase A inhibitors, inhibited the enhancing effect of TS on LPS/IFN-induced NO production. Furthermore, TS enhanced the amount of PKCalpha in VSMC. From these results, we concluded that the enhancing effect of LPS/IFN-induced NO production was caused by upregulation of PKC in VSMC.
引用
收藏
页码:2367 / 2372
页数:6
相关论文
共 34 条
[11]   Regulation of inducible nitric oxide synthase gene expression in vascular smooth muscle cells [J].
Hecker, M ;
Cattaruzza, M ;
Wagner, AH .
GENERAL PHARMACOLOGY, 1999, 32 (01) :9-16
[12]   Effect of hypoxia on nitric oxide production and its synthase gene expression in rat smooth muscle cells [J].
Hong, Y ;
Suzuki, S ;
Yatoh, S ;
Mizutani, M ;
Nakajima, T ;
Bannai, S ;
Sato, H ;
Soma, M ;
Okuda, Y ;
Yamada, N .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 268 (02) :329-332
[13]   Nitric oxide and the proliferation of vascular smooth muscle cells [J].
Jeremy, JY ;
Rowe, D ;
Emsley, AM ;
Newby, AC .
CARDIOVASCULAR RESEARCH, 1999, 43 (03) :580-594
[14]  
Kim SJ, 1998, J CELL SCI, V111, P435
[15]   Superoxide is responsible for apoptosis in rat vascular smooth muscle cells induced by α-tocopheryl hemisuccinate [J].
Kogure, K ;
Morita, M ;
Nakashima, S ;
Hama, S ;
Tokumura, A ;
Fukuzawa, K .
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 2001, 1528 (01) :25-30
[16]  
KRAMER IM, 1988, J BIOL CHEM, V263, P2352
[17]   Inhibition of NF-κB transcriptional activity by α-tocopheryl succinate [J].
Nakamura, Tetsuya ;
Goto, Masaki ;
Matsumoto, Akira ;
Tanaka, Isao .
BIOFACTORS, 1998, 7 (1-2) :21-30
[18]   α-tocopheryl succinate-induced apoptosis in Jurkat T cells involves caspase-3 activation, and both lysosomal and mitochondrial destabilisation [J].
Neuzil, J ;
Svensson, I ;
Weber, T ;
Weber, C ;
Brunk, UT .
FEBS LETTERS, 1999, 445 (2-3) :295-300
[19]   Vitamin E analogues as inducers of apoptosis: implications for their potential antineoplastic role [J].
Neuzil, J ;
Weber, T ;
Terman, A ;
Weber, C ;
Brunk, UT .
REDOX REPORT, 2001, 6 (03) :143-151
[20]   Induction of cancer cell apoptosis by α-tocopheryl succinate:: molecular pathways and structural requirements [J].
Neuzil, J ;
Weber, T ;
Schröder, A ;
Lu, M ;
Ostermann, G ;
Gellert, N ;
Mayne, GC ;
Olejnicka, B ;
Nègre-Salvayre, A ;
Stícha, M ;
Coffey, RJ ;
Weber, C .
FASEB JOURNAL, 2001, 15 (02) :403-415