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RISS 인기검색어
- 검색키워드
- 저자 : Yabe-Nishimura, Chihiro (검색결과 4 건)
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Kim, Hyo Jung,Ham, Sun Ah,Kim, Sung Uk,Hwang, Jin-Yong,Kim, Jae-Hwan,Chang, Ki Churl,Yabe-Nishimura, Chihiro,Kim, Jin-Hoi,Seo, Han Geuk Ovid Technologies Wolters Kluwer -American Heart A 2008 Circulation research Vol.102 No.2
<P>The peroxisome proliferator-activated receptor (PPAR)delta has been implicated in the pathogenesis of atherogenic disorders. However, its physiological roles and functions in vascular smooth muscle cells (VSMCs) remain relatively unclear. In the present study, we show that the gene encoding transforming growth factor (TGF)-beta1 is a PPARdelta target in VSMCs. The PPARdelta activator GW501516 upregulates TGF-beta1 expression in a dose- and time-dependent manner. This induction is attenuated significantly by the presence of small interfering RNA against PPARdelta or GW9662, an inhibitor of PPARdelta. Furthermore, activated PPARdelta induces TGF-beta1 promoter activity by binding to the direct repeat-1 response element TGF-beta1-direct repeat-1. Mutations in the 5' or 3' half-sites of the response element totally abrogate transcriptional activation and PPARdelta binding, which suggests that this site is a novel type of PPARdelta response element. In addition, ligand-activated PPARdelta attenuated the promoter activity and expression of monocyte chemoattractant protein-1 induced by interleukin-1beta. These effects were significantly reduced in the presence of small interfering RNA against PPARdelta, anti-TGF-beta1 antibody, or a TGF-beta type I receptor inhibitor. Decreased monocyte chemoattractant protein-1 expression induced by PPARdelta was mediated by the effector of TGF-beta1, Smad3. Finally, administration of GW501516 to mice upregulated TGF-beta1, whereas the expression of proinflammatory genes including monocyte chemoattractant protein-1 was significantly attenuated in the thoracic aorta. Taken together, these results demonstrate the presence of a novel TGF-beta1-mediated pathway in the antiinflammatory activities of PPARdelta.</P>
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Kim, Hyo Jung,Kim, Min Young,Jin, Hana,Kim, Hyun Joon,Kang, Sang Soo,Kim, Hye Jung,Lee, Jae Heun,Chang, Ki Churl,Hwang, Jin-Yong,Yabe-Nishimura, Chihiro,Kim, Jin-Hoi,Seo, Han Geuk Ovid Technologies Wolters Kluwer -American Heart A 2009 Circulation research Vol.105 No.1
<P>Homeostasis of the extracellular matrix and apoptosis of vascular smooth muscle cells (VSMCs) are key components in the regulation of the stability of atherosclerotic plaques. Here, we demonstrate that peroxisome proliferator-activated receptor (PPAR)delta regulates extracellular matrix synthesis and degradation through transforming growth factor-beta1 and its effector, Smad3. Activation of PPARdelta strongly amplified the expression of types I and III collagen, fibronectin, elastin, and TIMP-3 (tissue inhibitor of metalloproteinases 3), but not of TIMP-1, matrix metalloproteinase-2 or -9. The effect of PPARdelta on the expression of type III collagen was dually regulated by the direct binding of PPARdelta and Smad3 to a direct repeat-1 site and a Smad-binding element, respectively, in the type III collagen gene promoter. The activation of PPARdelta attenuated apoptotic cell death in VSMCs induced by oxidized low-density lipoprotein, and similar antiapoptotic effects were observed on treatment of cells with exogenous type I and/or III collagen. Administration of a PPARdelta ligand GW501516 to mice also suppressed elastase-induced cell death of aortic VSMCs. These results suggest that PPARdelta-induced upregulation of extracellular matrix proteins exerts an antiapoptotic effect, thereby maintaining the stability of atherosclerotic plaques. Specific ligands of PPARdelta may aid in the therapeutic intervention of atherosclerosis by improving plaque stability and patient prognosis.</P>
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Interaction of NADPH oxidase 1 with Toll-like receptor 2 induces migration of smooth muscle cells
Lee, Jee Hyun,Joo, Jung Hee,Kim, Jinoh,Lim, Hee Jung,Kim, Sunah,Curtiss, Linda,Seong, Je Kyung,Cui, Wenhao,Yabe-Nishimura, Chihiro,Bae, Yun Soo Oxford University Press 2013 Cardiovascular research Vol.99 No.3
<P><B>Aims</B></P><P>NADPH oxidase (Nox) isozymes that generate intracellular reactive oxygen species (ROS) and Toll-like receptor 2 (TLR2), an inflammatory mediator, are both involved in the development of atherosclerotic lesions. To identify the molecular connection between TLR2 and Nox isozymes in vascular remodelling, we analysed generation of ROS and pro-inflammatory cytokines in aortic smooth muscle cells from Nox1-deficient mice in response to the synthetic triacylated lipoprotein Pam3CSK, a TLR2 agonist.</P><P><B>Methods and results</B></P><P>We showed that TLR2 signalling stimulates progression of the pro-inflammatory phenotype in mouse aortic smooth muscle cells (MASMCs) through activation of Nox1. We demonstrated the interaction of TLR2 with Nox1 using yeast two-hybrid and co-immunoprecipitation assays. MASMCs from Nox1-deficient mice failed to generate of ROS in response to Pam3CSK4, indicating that Nox1 is essential for TLR2-dependent production of ROS. We also found that Pam3CSK4 stimulated migration of MASMCs from wild-type mice in a Transwell system, but MASMCs from Nox1-deficient mice failed to show this response. Wild-type MASMCs produced matrix metalloprotease 2 in response to Pam3CSK4, whereas Nox1-deficient MASMCs failed to generate this protease. Moreover, stimulation of MASMCs with Pam3CSK4 resulted in increased expression of the pro-inflammatory cytokine macrophage inflammatory protein 2 in a Nox1-dependent manner, leading to enhanced monocyte-endothelial cell adhesion and trans-endothelial migration of U937 cells.</P><P><B>Conclusion</B></P><P>These data suggest that Nox1 plays an important role in TLR2-mediated intracellular H<SUB>2</SUB>O<SUB>2</SUB> generation, activation of matrix metalloprotease 2, and secretion of pro-inflammatory cytokines, which in turn stimulate MASMC migration and vascular remodelling.</P>
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Kang, Eun Sil,Kim, Gil Hyeong,Woo, Im Sun,Kim, Hyo Jung,Eun, So Young,Ham, Sun Ah,Jin, Hana,Kim, Min Young,Park, Myung Hyun,Kim, Hye Jung,Chang, Ki Churl,Lee, Jae Heun,Kim, Jin-Hoi,Yabe-Nishimura, Chi Harwood Academic ; Distributed by STBS Ltd 2008 Free radical research Vol.42 No.11
<P>Aldose reductase (AR) is abundantly expressed in a variety of cell lineages and has been implicated in the cellular response against oxidative stress. However, the exact functional role of AR against oxidative stress remains relatively unclear. This study investigated the role of AR in acrolein- or hydrogen peroxide-induced apoptosis using the J774.A.1 macrophage cell line. Ablation of AR with a small interference RNA or inhibition of AR activity significantly enhanced the acrolein- or hydrogen peroxide-induced generation of reactive oxygen species and aldehydes, leading to increased apoptotic cell death. Blockade of AR activity in J774A.1 cells markedly augmented the acrolein- or hydrogen peroxide-induced translocation of Bax to mitochondria along with reduced Bcl-2 and increased release of cytochrome c from the mitochodria. Taken together, these findings indicate that AR plays an important role in the cellular response against oxidative stress, by sequestering the reactive molecules generated in cells exposed to toxic substances.</P>
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