Reactive Oxygen Species-Mediated Signaling Pathways in Angiotensin II-Induced MCP- Expression of Proximal Tubular Cells

DOI Web Site PubMed 被引用文献3件
  • Chiaki Tanifuji
    Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
  • Yusuke Suzuki
    Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
  • Wong Mu Geot
    Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
  • Satoshi Horikoshi
    Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
  • Takeshi Sugaya
    Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
  • Marta Ruiz-Ortega
    Renal and Vascular Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain.
  • Jesus Egido
    Renal and Vascular Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain.
  • Andyasuhiko Tomino
    Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.

書誌事項

公開日
2005-09
資源種別
journal article
DOI
  • 10.1089/ars.2005.7.1261
公開者
SAGE Publications

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説明

Angiotensin II (AngII) has pleiotropic effects, the most well known of which is the generation of reactive oxygen species (ROS) and chemokines in inflammatory lesions. Monocyte chemoattractant protein-1 (MCP-1) is considered a major chemokine in the pathogenesis of kidney diseases. We examined signaling pathways of AngII-induced MCP-1 expression and the role of ROS in the murine proximal tubular cells (mProx) using various inhibitors. Furthermore, we compared the signaling pathways between mProx and mesangial cells (MC). AngII-induced MCP-1 protein expression in mProx at 6 h was largely blocked by ROS (N-acetylcysteine; 82 +/- 14%), Ras (N-acetyl-S-trans,trans-farnesyl-L-cysteine; 82 +/- 13%), and nuclear factor-kappaB (NF-kappaB) (parthenolide; 89 +/- 7.9%) inhibitors. Both AT1 receptor (AT1R) (Olmesartan; 41 +/- 12%) and the AT2R (PD123319; 24 +/- 11%) antagonists partially blocked the MCP-1 expression. Furthermore, mitogen-activated protein kinase (MAPK) pathways were also implicated in this protein expression, but it is less dependent on ROS/Ras pathways. In MC, protein kinase (calphostin C; 84 +/- 2.8%) and NF-kappaB (89 +/- 1.4%) inhibitors attenuated acute AngII-induced MCP-1 expression stronger than ROS/Ras inhibitors (1.0 +/- 0.9/29 +/- 9.5%). MAPK pathways, especially p38 MAPK, were involved in MC more than in mProx. AT1R (69 +/- 8.6%) and AT2R (57 +/- 21%) antagonists also were blocked. We suggested that, although NF-kappaB activation has a critical role, signaling pathways are different between mProx and MC. ROS-mediated signaling in mProx may have more contribution to AngII-induced inflammatory responses than to those in MC.

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