PMID- 14684844
OWN - NLM
STAT- MEDLINE
DCOM- 20041110
LR  - 20220317
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 18
IP  - 3
DP  - 2004 Mar
TI  - Regulation of inhibitory protein-kappaB and monocyte chemoattractant protein-1 by 
      angiotensin II type 2 receptor-activated Src homology protein tyrosine 
      phosphatase-1 in fetal vascular smooth muscle cells.
PG  - 666-78
AB  - In the present study we examined the effects of angiotensin II (Ang II) type 2 
      (AT(2)) receptor stimulation on AT(1) receptor-mediated monocyte chemoattractant 
      protein-1 (MCP-1) expression and the possible mechanisms of AT(2) 
      receptor-mediated signaling in cultured rat fetal vascular smooth muscle cells, 
      which express both AT(1) and AT(2) receptors. Ang II stimulation induced MCP-1 
      mRNA expression as well as an increase in nuclear factor-kappaB (NF-kappaB) 
      binding to the corresponding cis DNA element of the MCP-1 promoter region and a 
      decrease in the cytosolic inhibitory protein-kappaB (IkappaB) protein level via 
      AT(1) receptor stimulation, whereas stimulation of the AT(2) receptor decreased 
      Ang II-induced MCP-1 expression, NF-kappaB DNA binding, and IkappaB degradation, 
      suggesting that activation of the AT(2) receptor attenuated AT(1) 
      receptor-mediated MCP-1 expression via a decrease in NF-kappaB DNA binding and an 
      increase in IkappaB stability. Moreover, we demonstrated that AT(2) receptor 
      stimulation attenuated TNFalpha-mediated NF-kappaB activation and MCP-1 
      expression. A tyrosine phosphatase inhibitor, orthovanadate, attenuated the AT(2) 
      receptor-mediated increase in IkappaB protein. Moreover, we observed that two 
      IkappaB subunits (IkappaBalpha and IkappaBbeta) were tyrosine-phosphorylated 
      after Ang II stimulation. Transfection of a dominant-negative Src homology 
      protein tyrosine phosphatase-1 mutant into vascular smooth muscle cells inhibited 
      the AT(2) receptor-mediated increase in IkappaB, leading to a significant 
      increase in AT(1) receptor-induced NF-kappaB activation and MCP-1 expression. 
      Taken together, our results demonstrated that AT(2) receptor stimulation 
      attenuated MCP-1 expression via IkappaB stabilization, and Src homology protein 
      tyrosine phosphatase-1 might play a critical role in the transcriptional 
      regulation of MCP-1 expression through the control of IkappaB protein stability.
FAU - Wu, Lan
AU  - Wu L
AD  - Department of Medical Biochemistry, Ehime University School of Medicine, 
      Shigenobu, Onsen-gun, Ehime 791-0295, Japan.
FAU - Iwai, Masaru
AU  - Iwai M
FAU - Li, Zhen
AU  - Li Z
FAU - Shiuchi, Tetsuya
AU  - Shiuchi T
FAU - Min, Li-Juan
AU  - Min LJ
FAU - Cui, Tai-Xing
AU  - Cui TX
FAU - Li, Jian-Mei
AU  - Li JM
FAU - Okumura, Midori
AU  - Okumura M
FAU - Nahmias, Clara
AU  - Nahmias C
FAU - Horiuchi, Masatsugu
AU  - Horiuchi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20031218
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Angiotensin II Type 2 Receptor Blockers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (I kappa B beta protein)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (Imidazoles)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Oligopeptides)
RN  - 0 (Pyridines)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 11128-99-7 (Angiotensin II)
RN  - 127060-75-7 (CGP 42112A)
RN  - 130663-39-7 (PD 123319)
RN  - EC 3.1.3.16 (Protein Phosphatase 1)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 6)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatases)
RN  - EC 3.1.3.48 (Ptpn6 protein, rat)
SB  - IM
MH  - Angiotensin II/antagonists & inhibitors/pharmacology
MH  - Angiotensin II Type 1 Receptor Blockers
MH  - Angiotensin II Type 2 Receptor Blockers
MH  - Animals
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cytosol/drug effects/metabolism
MH  - Gene Expression Regulation
MH  - I-kappa B Proteins/drug effects/genetics/*metabolism
MH  - Imidazoles/pharmacology
MH  - Intracellular Signaling Peptides and Proteins
MH  - Muscle, Smooth, Vascular/cytology/embryology/*metabolism
MH  - Mutation
MH  - NF-kappa B
MH  - Oligopeptides/pharmacology
MH  - Protein Phosphatase 1
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 1
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 6
MH  - Protein Tyrosine Phosphatases/drug effects/genetics/*metabolism
MH  - Pyridines/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, Angiotensin, Type 1/drug effects/metabolism
MH  - Receptor, Angiotensin, Type 2/drug effects/*metabolism
EDAT- 2003/12/20 05:00
MHDA- 2004/11/13 09:00
CRDT- 2003/12/20 05:00
PHST- 2003/12/20 05:00 [pubmed]
PHST- 2004/11/13 09:00 [medline]
PHST- 2003/12/20 05:00 [entrez]
AID - me.2003-0053 [pii]
AID - 10.1210/me.2003-0053 [doi]
PST - ppublish
SO  - Mol Endocrinol. 2004 Mar;18(3):666-78. doi: 10.1210/me.2003-0053. Epub 2003 Dec 
      18.