PMID- 26767865
OWN - NLM
STAT- MEDLINE
DCOM- 20170117
LR  - 20181113
IS  - 2005-6648 (Electronic)
IS  - 1226-3303 (Print)
IS  - 1226-3303 (Linking)
VI  - 31
IP  - 1
DP  - 2016 Jan
TI  - Angiotensin III increases monocyte chemoattractant protein-1 expression in 
      cultured human proximal tubular epithelial cells.
PG  - 116-24
LID - 10.3904/kjim.2016.31.1.116 [doi]
AB  - 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.
FAU - Kim, Hyung Wook
AU  - Kim HW
AD  - Division of Nephrology, Department of Internal Medicine, College of Medicine, St. 
      Vincent's Hospital, The Catholic University of Korea, Suwon, Korea.
FAU - Kim, Young Ok
AU  - Kim YO
AD  - Division of Nephrology, Department of Internal Medicine, College of Medicine, 
      Uijeongbu St. Mary's Hospital, The Catholic University of Korea, Uijeongbu, 
      Korea.
FAU - Yoon, Sun Ae
AU  - Yoon SA
AD  - Division of Nephrology, Department of Internal Medicine, College of Medicine, 
      Uijeongbu St. Mary's Hospital, The Catholic University of Korea, Uijeongbu, 
      Korea.
FAU - Han, Jeong-Sun
AU  - Han JS
AD  - Renal Research Laboratory, Division of Nephrology, Department of Internal 
      Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
FAU - Chun, Hyun-Bae
AU  - Chun HB
AD  - Department of Medicine, Stony Brook University of New York, Stony Brook, NY, USA.
FAU - Kim, Young Soo
AU  - Kim YS
AD  - Division of Nephrology, Department of Internal Medicine, College of Medicine, 
      Uijeongbu St. Mary's Hospital, The Catholic University of Korea, Uijeongbu, 
      Korea.
LA  - eng
PT  - Journal Article
DEP - 20151228
PL  - Korea (South)
TA  - Korean J Intern Med
JT  - The Korean journal of internal medicine
JID - 8712418
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Transcription Factor AP-1)
RN  - 12687-51-3 (Angiotensin III)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Angiotensin II Type 1 Receptor Blockers/pharmacology
MH  - Angiotensin III/*pharmacology
MH  - Cell Line
MH  - Chemokine CCL2/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Epithelial Cells/*drug effects/metabolism
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism
MH  - Kidney Tubules, Proximal/*drug effects/metabolism
MH  - Phosphorylation
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Signal Transduction/drug effects
MH  - Time Factors
MH  - Transcription Factor AP-1/metabolism
MH  - Up-Regulation
MH  - p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism
PMC - PMC4712415
OTO - NOTNLM
OT  - Angiotensin III
OT  - Chemokine CCL2
OT  - Kidney tubules
OT  - Mitogen-activated protein kinases
OT  - Transcription factors
COIS- No potential conflict of interest relevant to this article was reported.
EDAT- 2016/01/16 06:00
MHDA- 2017/01/18 06:00
PMCR- 2016/01/01
CRDT- 2016/01/16 06:00
PHST- 2014/07/02 00:00 [received]
PHST- 2014/08/26 00:00 [revised]
PHST- 2014/08/26 00:00 [accepted]
PHST- 2016/01/16 06:00 [entrez]
PHST- 2016/01/16 06:00 [pubmed]
PHST- 2017/01/18 06:00 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - kjim-31-1-116 [pii]
AID - 10.3904/kjim.2016.31.1.116 [doi]
PST - ppublish
SO  - Korean J Intern Med. 2016 Jan;31(1):116-24. doi: 10.3904/kjim.2016.31.1.116. Epub 
      2015 Dec 28.