The Korean journal of internal medicine

  • 제31권1호
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  • Pages.116-124
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  • 2016
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  • 1226-3303(pISSN)
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  • 2005-6648(eISSN)
대한내과학회 (The Korean Association of Internal Medicine)
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Angiotensin III increases monocyte chemoattractant protein-1 expression in cultured human proximal tubular epithelial cells

  • Kim, Hyung Wook (Division of Nephrology, Department of Internal Medicine, College of Medicine, St. Vincent's Hospital, The Catholic University of Korea) ;
  • Kim, Young Ok (Division of Nephrology, Department of Internal Medicine, College of Medicine, Uijeongbu St. Mary's Hospital, The Catholic University of Korea) ;
  • Yoon, Sun Ae (Division of Nephrology, Department of Internal Medicine, College of Medicine, Uijeongbu St. Mary's Hospital, The Catholic University of Korea) ;
  • Han, Jeong-Sun (Renal Research Laboratory, Division of Nephrology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea) ;
  • Chun, Hyun-Bae (Department of Medicine, Stony Brook University of New York) ;
  • Kim, Young Soo (Division of Nephrology, Department of Internal Medicine, College of Medicine, Uijeongbu St. Mary's Hospital, The Catholic University of Korea)
  • 투고 : 2014.07.02
  • 심사 : 2014.08.26
  • 발행 : 2016.01.01
⟨ 이전 논문 다음 논문 ⟩

초록

Background/Aims: We investigated whether angiotensin III (Ang III) is involved in monocyte recruitment through regulation of the chemokine monocyte chemoattractant protein-1 (MCP-1) in cultured human proximal tubular epithelial cells (HK-2 cells). Methods: We measured MCP-1 levels in HK-2 cells that had been treated with various concentrations of Ang III and Ang II type-1 (AT1) receptor antagonists at various time points. The phosphorylation states of p38, c-Jun N-terminal kinases (JNK), and extracellular-signal-regulated kinases were measured in Ang III-treated cells to explore the mitogen-activated protein kinase (MAPK) pathway. MCP-1 levels in HK-2 cell-conditioned media were measured after pre-treatment with the transcription factor inhibitors curcumin or pyrrolidine dithiocarbamate. Results: Ang III increased MCP-1 protein production in dose- and time-dependent manners in HK-2 cells, which was inhibited by the AT1 receptor blocker losartan. p38 MAPK activity increased significantly in HK-2 cells exposed to Ang III for 30 minutes, and was sustained at higher levels after 60 minutes (p < 0.05). Total phosphorylated JNK protein levels tended to increase 20 minutes after stimulation with Ang III. Pre-treatment with a p38 inhibitor, a JNK inhibitor, or curcumin significantly inhibited Ang III-induced MCP-1 production. Conclusions: Ang III increases MCP-1 synthesis via stimulation of intracellular p38 and JNK MAPK signaling activity and subsequent activated protein-1 transcriptional activity in HK-2 cells.

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