PMID- 16115031
OWN - NLM
STAT- MEDLINE
DCOM- 20060104
LR  - 20161124
IS  - 1523-0864 (Print)
IS  - 1523-0864 (Linking)
VI  - 7
IP  - 9-10
DP  - 2005 Sep-Oct
TI  - Reactive oxygen species-mediated signaling pathways in angiotensin II-induced 
      MCP-1 expression of proximal tubular cells.
PG  - 1261-8
AB  - 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.
FAU - Tanifuji, Chiaki
AU  - Tanifuji C
AD  - Division of Nephrology, Department of Internal Medicine, Juntendo University 
      School of Medicine, Tokyo, Japan.
FAU - Suzuki, Yusuke
AU  - Suzuki Y
FAU - Geot, Wong Mu
AU  - Geot WM
FAU - Horikoshi, Satoshi
AU  - Horikoshi S
FAU - Sugaya, Takeshi
AU  - Sugaya T
FAU - Ruiz-Ortega, Marta
AU  - Ruiz-Ortega M
FAU - Egido, Jesus
AU  - Egido J
FAU - Tomino, Yasuhiko
AU  - Tomino Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Angiotensin II Type 2 Receptor Blockers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Imidazoles)
RN  - 0 (NF-kappa B)
RN  - 0 (Naphthalenes)
RN  - 0 (Pyridines)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tetrazoles)
RN  - 11128-99-7 (Angiotensin II)
RN  - 130663-39-7 (PD 123319)
RN  - 8W1IQP3U10 (olmesartan)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - I271P23G24 (calphostin C)
SB  - IM
MH  - Angiotensin II/*physiology
MH  - Angiotensin II Type 1 Receptor Blockers/pharmacology
MH  - Angiotensin II Type 2 Receptor Blockers
MH  - Animals
MH  - Blotting, Western
MH  - Cell Line
MH  - Chemokine CCL2/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Imidazoles/pharmacology
MH  - Kidney/cytology
MH  - Kidney Tubules/*cytology
MH  - Mesangial Cells/cytology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - NF-kappa B/metabolism
MH  - Naphthalenes/pharmacology
MH  - Oxidation-Reduction
MH  - Prognosis
MH  - Pyridines/pharmacology
MH  - *Reactive Oxygen Species
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - *Signal Transduction
MH  - Tetrazoles/pharmacology
MH  - Time Factors
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2005/08/24 09:00
MHDA- 2006/01/05 09:00
CRDT- 2005/08/24 09:00
PHST- 2005/08/24 09:00 [pubmed]
PHST- 2006/01/05 09:00 [medline]
PHST- 2005/08/24 09:00 [entrez]
AID - 10.1089/ars.2005.7.1261 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2005 Sep-Oct;7(9-10):1261-8. doi: 10.1089/ars.2005.7.1261.