PMID- 17611196
OWN - NLM
STAT- MEDLINE
DCOM- 20071029
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 282
IP  - 35
DP  - 2007 Aug 31
TI  - Role of MAPK phosphatase-1 in the induction of monocyte chemoattractant protein-1 
      during the course of adipocyte hypertrophy.
PG  - 25445-52
AB  - Monocyte chemoattractant protein-1 (MCP-1), an important chemokine whose 
      expression is increased during the course of obesity, plays a role in macrophage 
      infiltration into obese adipose tissue. This study was designed to elucidate the 
      role of mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) in the 
      induction of MCP-1 during the course of adipocyte hypertrophy. We examined the 
      time course of MKP-1 and MCP-1 mRNA expression and extracellular signal-regulated 
      kinase (ERK) phosphorylation in the adipose tissue from mice rendered mildly 
      obese by a short term high fat diet. We also studied the role of MKP-1 in the 
      induction of MCP-1 in 3T3-L1 adipocytes during the course of adipocyte 
      hypertrophy. MCP-1 mRNA expression was increased, followed by ERK activation and 
      down-regulation of MKP-1, an inducible dual specificity phosphatase to inactivate 
      ERK, in the adipose tissue at the early stage of obesity induced by a short term 
      high fat diet, when macrophages are not infiltrated. Down-regulation of MKP-1 
      preceded ERK activation and increased production of MCP-1 in 3T3-L1 adipocytes in 
      vitro during the course of adipocyte hypertrophy. Adenovirus-mediated restoration 
      of MKP-1 in hypertrophied 3T3-L1 adipocytes reduced the otherwise increased ERK 
      phosphorylation, thereby leading to the significant reduction of MCP-1 mRNA 
      expression. This study provides evidence that the down-regulation of MKP-1 is 
      critical for increased production of MCP-1 during the course of adipocyte 
      hypertrophy.
FAU - Ito, Ayaka
AU  - Ito A
AD  - Department of Molecular Medicine and Metabolism, Medical Research Institute, 
      Tokyo Medical and Dental University, and Department of Medicine, National 
      Cardiovascular Center Hospital, Osaka, Japan.
FAU - Suganami, Takayoshi
AU  - Suganami T
FAU - Miyamoto, Yoshihiro
AU  - Miyamoto Y
FAU - Yoshimasa, Yasunao
AU  - Yoshimasa Y
FAU - Takeya, Motohiro
AU  - Takeya M
FAU - Kamei, Yasutomi
AU  - Kamei Y
FAU - Ogawa, Yoshihiro
AU  - Ogawa Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070703
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 3.1.3.16 (Phosphoprotein Phosphatases)
RN  - EC 3.1.3.16 (Protein Phosphatase 1)
RN  - EC 3.1.3.48 (Dual Specificity Phosphatase 1)
RN  - EC 3.1.3.48 (Dusp1 protein, mouse)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatases)
SB  - IM
MH  - Adipocytes/*enzymology/pathology
MH  - Adipose Tissue/enzymology/pathology
MH  - Animals
MH  - Cell Cycle Proteins/*biosynthesis
MH  - Cell Movement
MH  - Chemokine CCL2/*biosynthesis
MH  - Down-Regulation
MH  - Dual Specificity Phosphatase 1
MH  - Enzyme Activation
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - *Gene Expression Regulation, Enzymologic
MH  - Hypertrophy
MH  - Immediate-Early Proteins/*biosynthesis
MH  - Macrophages/metabolism/pathology
MH  - Male
MH  - Mice
MH  - Obesity/enzymology/pathology
MH  - Phosphoprotein Phosphatases/*biosynthesis
MH  - Phosphorylation
MH  - Protein Phosphatase 1
MH  - Protein Tyrosine Phosphatases/*biosynthesis
MH  - RNA, Messenger/biosynthesis
MH  - Time Factors
MH  - Up-Regulation
EDAT- 2007/07/06 09:00
MHDA- 2007/10/30 09:00
CRDT- 2007/07/06 09:00
PHST- 2007/07/06 09:00 [pubmed]
PHST- 2007/10/30 09:00 [medline]
PHST- 2007/07/06 09:00 [entrez]
AID - S0021-9258(20)74618-1 [pii]
AID - 10.1074/jbc.M701549200 [doi]
PST - ppublish
SO  - J Biol Chem. 2007 Aug 31;282(35):25445-52. doi: 10.1074/jbc.M701549200. Epub 2007 
      Jul 3.