PMID- 16705055
OWN - NLM
STAT- MEDLINE
DCOM- 20061024
LR  - 20151119
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 291
IP  - 4
DP  - 2006 Oct
TI  - Angiotensin II induces monocyte chemoattractant protein-1 expression via a 
      nuclear factor-kappaB-dependent pathway in rat preadipocytes.
PG  - E771-8
AB  - Both monocyte chemoattractant protein-1 (MCP-1), a member of chemokine family, 
      and angiotensinogen, a precursor of angiotensin (ANG) II, are produced by adipose 
      tissue and increased in obese state. MCP-1 has been shown to decrease 
      insulin-stimulated glucose uptake and several adipogenic genes expression in 
      adipocytes in vitro, suggesting its pathophysiological significance in obesity. 
      However, the pathophysiological interaction between MCP-1 and ANG II in adipose 
      tissue remains unknown. The present study was undertaken to investigate the 
      potential mechanisms by which ANG II affects MCP-1 gene expression in rat primary 
      cultured preadipocytes and adipose tissue in vivo. ANG II significantly increased 
      steady-state MCP-1 mRNA levels in a time- and dose-dependent manner. The ANG 
      II-induced MCP-1 mRNA and protein expression was completely abolished by ANG II 
      type 1 (AT1)-receptor antagonist (valsartan). An antioxidant/NF-kappaB inhibitor 
      (pyrrolidine dithiocarbamate) and an inhibitor of 1kappaB-alpha phosphorylation 
      (Bay 11-7085) also blocked ANG II-induced MCP-1 mRNA expression. ANG II induced 
      translocation of NF-kappaB p65 subunit from cytoplasm to nucleus by 
      immunocytochemical study. Luciferase assay using reporter constructs containing 
      MCP-1 promoter region revealed that two NF-kappaB binding sites in its enhancer 
      region were essential for the ANG II-induced promoter activities. Furthermore, 
      basal mRNA and protein of MCP-1 during preadipocyte differentiation were 
      significantly greater in preadipocytes than in differentiated adipocytes, whose 
      effect was more pronounced in the presence of ANG II. Exogenous administration of 
      ANG II to rats led to increased MCP-1 expression in epididymal, subcutaneous, and 
      mesenteric adipose tissue. In conclusion, our present study demonstrates that ANG 
      II increases MCP-1 gene expression via ANG II type 1 receptor-mediated and 
      NF-kappaB-dependent pathway in rat preadipocytes as well as adipose MCP-1 
      expression in vivo. Thus the augmented MCP-1 expression by ANG II in 
      preadipocytes may provide a new link between obesity and cardiovascular disease.
FAU - Tsuchiya, Kyoichiro
AU  - Tsuchiya K
AD  - Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental 
      University Graduate School, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8513, Japan.
FAU - Yoshimoto, Takanobu
AU  - Yoshimoto T
FAU - Hirono, Yuki
AU  - Hirono Y
FAU - Tateno, Toru
AU  - Tateno T
FAU - Sugiyama, Toru
AU  - Sugiyama T
FAU - Hirata, Yukio
AU  - Hirata Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060516
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Antioxidants)
RN  - 0 (BAY 11-7085)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitriles)
RN  - 0 (Pyrrolidines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Sulfones)
RN  - 0 (Tetrazoles)
RN  - 0 (Thiocarbamates)
RN  - 11128-99-7 (Angiotensin II)
RN  - 25769-03-3 (pyrrolidine dithiocarbamic acid)
RN  - 80M03YXJ7I (Valsartan)
RN  - HG18B9YRS7 (Valine)
SB  - IM
MH  - Adipocytes/drug effects/metabolism
MH  - Adipose Tissue/drug effects/*metabolism
MH  - Angiotensin II/antagonists & inhibitors/*pharmacology/physiology
MH  - Angiotensin II Type 1 Receptor Blockers/antagonists & inhibitors/pharmacology
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Cell Differentiation/physiology
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Humans
MH  - Male
MH  - NF-kappa B/antagonists & inhibitors/*metabolism
MH  - Nitriles/pharmacology
MH  - Obesity/metabolism
MH  - Promoter Regions, Genetic
MH  - Pyrrolidines/pharmacology
MH  - RNA, Messenger/chemistry/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, Angiotensin, Type 1/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sulfones/pharmacology
MH  - Tetrazoles/pharmacology
MH  - Thiocarbamates/pharmacology
MH  - Transcription, Genetic
MH  - Valine/analogs & derivatives/pharmacology
MH  - Valsartan
EDAT- 2006/05/18 09:00
MHDA- 2006/10/25 09:00
CRDT- 2006/05/18 09:00
PHST- 2006/05/18 09:00 [pubmed]
PHST- 2006/10/25 09:00 [medline]
PHST- 2006/05/18 09:00 [entrez]
AID - 00560.2005 [pii]
AID - 10.1152/ajpendo.00560.2005 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2006 Oct;291(4):E771-8. doi: 
      10.1152/ajpendo.00560.2005. Epub 2006 May 16.