PMID- 9797345
OWN - NLM
STAT- MEDLINE
DCOM- 19981124
LR  - 20220408
IS  - 0009-7330 (Print)
IS  - 0009-7330 (Linking)
VI  - 83
IP  - 9
DP  - 1998 Nov 2
TI  - Angiotensin II induces monocyte chemoattractant protein-1 gene expression in rat 
      vascular smooth muscle cells.
PG  - 952-9
AB  - Monocyte infiltration into the vessel wall, a key initial step in the process of 
      atherosclerosis, is mediated in part by monocyte chemoattractant protein-1 
      (MCP-1). Hypertension, particularly in the presence of an activated 
      renin-angiotensin system, is a major risk factor for the development of 
      atherosclerosis. To investigate a potential molecular basis for a link between 
      hypertension and atherosclerosis, we studied the effects of angiotensin II (Ang 
      II) on MCP-1 gene expression in rat aortic smooth muscle cells. Rat smooth muscle 
      cells treated with Ang II exhibited a dose-dependent increase in MCP-1 mRNA 
      accumulation that was prevented by the AT1 receptor antagonist losartan. Ang II 
      also activated MCP-1 gene transcription. Inhibition of NADH/NADPH oxidase, which 
      generates superoxide and H2O2, with diphenylene iodonium or apocynin decreased 
      Ang II-induced MCP-1 mRNA accumulation. Induction of MCP-1 gene expression by Ang 
      II was inhibited by catalase, suggesting a second messenger role for H2O2. The 
      tyrosine kinase inhibitor genistein and the mitogen-activated protein kinase 
      kinase inhibitor PD098059 inhibited Ang II-induced MCP-1 gene expression, 
      consistent with a mitogen-activated protein kinase-dependent signaling mechanism. 
      Ang II may thus promote atherogenesis by direct activation of MCP-1 gene 
      expression in vascular smooth muscle cells.
FAU - Chen, X L
AU  - Chen XL
AD  - Division of Cardiology, Department of Medicine, Emory University School of 
      Medicine, Atlanta, GA, USA.
FAU - Tummala, P E
AU  - Tummala PE
FAU - Olbrych, M T
AU  - Olbrych MT
FAU - Alexander, R W
AU  - Alexander RW
FAU - Medford, R M
AU  - Medford RM
LA  - eng
GR  - P01-HL-48667/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Multienzyme Complexes)
RN  - 0 (RNA, Messenger)
RN  - 11128-99-7 (Angiotensin II)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 1.6.- (NADH oxidase)
RN  - EC 1.6.- (NADH, NADPH Oxidoreductases)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Angiotensin Receptor Antagonists
MH  - Animals
MH  - Calcium-Calmodulin-Dependent Protein Kinases/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Gene Expression Regulation/*drug effects
MH  - Hydrogen Peroxide/pharmacology
MH  - Multienzyme Complexes/antagonists & inhibitors
MH  - Muscle, Smooth, Vascular/cytology/*drug effects/metabolism
MH  - NADH, NADPH Oxidoreductases/antagonists & inhibitors
MH  - Nitric Oxide/physiology
MH  - Protein-Tyrosine Kinases/physiology
MH  - RNA, Messenger/analysis
MH  - Rats
EDAT- 1998/10/31 00:00
MHDA- 1998/10/31 00:01
CRDT- 1998/10/31 00:00
PHST- 1998/10/31 00:00 [pubmed]
PHST- 1998/10/31 00:01 [medline]
PHST- 1998/10/31 00:00 [entrez]
AID - 10.1161/01.res.83.9.952 [doi]
PST - ppublish
SO  - Circ Res. 1998 Nov 2;83(9):952-9. doi: 10.1161/01.res.83.9.952.