PMID- 18164957
OWN - NLM
STAT- MEDLINE
DCOM- 20080312
LR  - 20201209
IS  - 0188-4409 (Print)
IS  - 0188-4409 (Linking)
VI  - 39
IP  - 2
DP  - 2008 Feb
TI  - ACE2 overexpression inhibits angiotensin II-induced monocyte chemoattractant 
      protein-1 expression in macrophages.
PG  - 149-54
LID - 10.1016/j.arcmed.2007.07.010 [doi]
AB  - BACKGROUND: The discovery of angiotensin-converting enzyme 2 (ACE2) has shed 
      light on the potential therapy for cardiovascular disease, owing to its key role 
      in the formation of vasoprotective peptide angiotensin (Ang 1-7) from angiotensin 
      (Ang) II. The aim of this study was to evaluate whether ACE2 overexpression could 
      protect human monocyte cell line (THP-1) macrophages from angiotensin II-induced 
      monocyte chemoattractant protein-1 (MCP-1) formation. METHODS: A truncated form 
      of mouse ACE2 (mACE2) was cloned into adenovirus vector (Ad-ACE2) and transfected 
      into THP-1. We examined expression of MCP-1 by administration of a selected Ang 
      (1-7) antagonist (A779) to show the effect of ACE2 overexpression on MCP-1 level 
      induced by AngII. RESULTS: AngII-induced MCP-1 expression increased obviously at 
      24 h and at the concentration of 10(-6) M. Transduction of THP-1 with Ad-ACE2 
      resulted in a viral increase in ACE2 activity. This was associated with a 
      significant attenuation of AngII-induced MCP-1 production by 39.6+/-4.0% in THP-1 
      (mean+/-SEM, n=3). Moreover, expression of MCP-1 increased by 35.1+/-4.2% in 
      Ad-ACE2 transfected THP-1 after incubation with Ang II and A779 compared to that 
      with AngII alone. Collectively, these results indicated that ACE2 overexpression 
      in the THP-1 attenuates AngII-induced MCP-1 production and that this reduction is 
      likely mediated by increased Ang (1-7) level. CONCLUSIONS: ACE2 overexpression 
      may provide a new therapeutic strategy for atherosclerosis by inhibiting MCP-1 
      production induced by AngII.
FAU - Guo, Yong-Jun
AU  - Guo YJ
AD  - Department of Cardiology, Shandong Provincial Hospital, Shandong University, 
      Jinan, PR China.
FAU - Li, Wei-Hua
AU  - Li WH
FAU - Wu, Rong
AU  - Wu R
FAU - Xie, Qiang
AU  - Xie Q
FAU - Cui, Lian-Qun
AU  - Cui LQ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071031
PL  - United States
TA  - Arch Med Res
JT  - Archives of medical research
JID - 9312706
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Peptide Fragments)
RN  - 11128-99-7 (Angiotensin II)
RN  - 9041-90-1 (Angiotensin I)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - EC 3.4.17.23 (ACE2 protein, human)
RN  - EC 3.4.17.23 (Ace2 protein, mouse)
RN  - EC 3.4.17.23 (Angiotensin-Converting Enzyme 2)
RN  - IJ3FUK8MOF (angiotensin I (1-7))
SB  - IM
MH  - Angiotensin I
MH  - Angiotensin II/antagonists & inhibitors/*metabolism/pharmacology
MH  - Angiotensin-Converting Enzyme 2
MH  - Animals
MH  - Cardiovascular Diseases/drug therapy/metabolism
MH  - Cell Line
MH  - Chemokine CCL2/*biosynthesis
MH  - Gene Expression Regulation/drug effects/*physiology
MH  - Humans
MH  - Mice
MH  - Peptide Fragments/antagonists & inhibitors/*metabolism/pharmacology
MH  - Peptidyl-Dipeptidase A/*metabolism
EDAT- 2008/01/01 09:00
MHDA- 2008/03/13 09:00
CRDT- 2008/01/01 09:00
PHST- 2007/06/03 00:00 [received]
PHST- 2007/07/17 00:00 [accepted]
PHST- 2008/01/01 09:00 [pubmed]
PHST- 2008/03/13 09:00 [medline]
PHST- 2008/01/01 09:00 [entrez]
AID - S0188-4409(07)00306-2 [pii]
AID - 10.1016/j.arcmed.2007.07.010 [doi]
PST - ppublish
SO  - Arch Med Res. 2008 Feb;39(2):149-54. doi: 10.1016/j.arcmed.2007.07.010. Epub 2007 
      Oct 31.