シミズ タツヤ   SHIMIZU Tatsuya
  清水 達也
   所属   研究施設 研究施設
   職種   教授
論文種別 原著
言語種別 英語
査読の有無 査読なし
表題 Lipopolysaccharide augments expression and secretion of vascular endothelial growth factor in rat ventricular myocytes.
掲載誌名 正式名:Biochemical and biophysical research communications
略  称:Biochem Biophys Res Commun
ISSNコード:(0006-291X)0006-291X(Linking)
掲載区分国外
出版社 Elsevier
巻・号・頁 268(2),657-62頁
著者・共著者 Sugishita Y†, Shimizu T, Yao A, Kinugawa K i, Nojiri T, Harada K, Matsui H, Nagai R, Takahashi T
発行年月 2000/02
概要 Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, is highly expressed in the myocardium under various stimuli including hypoxia and ischemia. On the other hand, lipopolysaccharide (LPS) causes systemic inflammatory response syndrome (SIRS), which consists of systemic pathophysiological changes related to vascular hyperpermeability. To test the hypothesis that VEGF is one of the important mediators of SIRS, we examined effects of LPS on the VEGF expression and secretion in cultured neonatal rat ventricular myocytes. LPS (10 microg/ml) rapidly (within 1 h) augmented the levels of VEGF mRNA in these cells. Pharmacological inhibition of nucleic factor-kappaB or tyrosine kinases did not affect the LPS-induced augmentation of VEGF mRNA expression, while these treatments markedly suppressed the up-regulation of inducible nitric oxide synthase (iNOS) expression by LPS. The VEGF concentrations in the conditioned media were also significantly increased by the LPS treatment of 6 h. In conclusion, LPS augments VEGF expression and secretion in rat ventricular myocytes, suggesting that VEGF may be involved in pathogenesis of SIRS. LPS may induce VEGF mRNA through the signaling pathways that are distinct from those responsible for the iNOS induction.
DOI 10.1006/bbrc.2000.2165
PMID 10679260