PMID- 25033895
OWN - NLM
STAT- MEDLINE
DCOM- 20150413
LR  - 20220330
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 34
IP  - 2
DP  - 2014
TI  - MCP-1 stimulates MMP-9 expression via ERK 1/2 and p38 MAPK signaling pathways in 
      human aortic smooth muscle cells.
PG  - 266-76
LID - 10.1159/000362997 [doi]
AB  - OBJECTIVE: We investigated the molecular mechanism underlying the role of 
      monocyte chemoattractant protein-1 (MCP-1) in the formation and development of 
      human abdominal aortic aneurysm (AAA). METHODS: We examined protein expression 
      profiles using a protein array and found that MCP-1 was the most highly expressed 
      protein in AAA tissues compared with normal aortas. To investigate the potential 
      mechanism of MCP-1 involvement in the pathogenesis of AAA, we treated human 
      aortic smooth muscle cells (HASMCs) with human recombinant MCP-1. RESULTS: MCP-1 
      was the most highly expressed protein in AAA tissues compared with normal aorta; 
      matrix metalloproteinase-9 (MMP-9) expression was also significantly increased. 
      Treatment with MCP-1 significantly increased the expression and activation of 
      MMP-9 and activated the three major mitogen activated protein kinases (MAPKs) 
      extracellular signal regulated kinase (ERK), c-Jun amino terminal kinase (JNK1/2) 
      and p38 MAPK. Furthermore, MCP-1-induced secretion of MMP-9 was inhibited by 
      U0126 (inhibitor of the ERK 1/2 pathway) and SB203580 (inhibitor of the p38 MAPK 
      pathway), but not SP600125 (inhibitor of the JNK1/2 pathway). CONCLUSION: These 
      data demonstrate that MCP-1 stimulates secretion of MMP-9 directly through the 
      ERK1/2 and p38 MAPK mediated pathways in HASMCs. Thus, inhibition of this 
      molecular mechanism might be a potential therapeutic target in the non-surgical 
      treatment of AAA.
CI  - (c) 2014 S. Karger AG, Basel.
FAU - Yang, Ci-Qiu
AU  - Yang CQ
AD  - Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen 
      University, Guangzhou, China.
FAU - Li, Wen
AU  - Li W
FAU - Li, Song-Qi
AU  - Li SQ
FAU - Li, Jie
AU  - Li J
FAU - Li, Yu-Wen
AU  - Li YW
FAU - Kong, Shu-Xin
AU  - Kong SX
FAU - Liu, Rui-Ming
AU  - Liu RM
FAU - Wang, Shen-Ming
AU  - Wang SM
FAU - Lv, Wei-Ming
AU  - Lv WM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140708
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA Primers)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Aorta/cytology/enzymology/*metabolism
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/*physiology
MH  - DNA Primers
MH  - Female
MH  - Humans
MH  - *MAP Kinase Signaling System
MH  - Male
MH  - Matrix Metalloproteinase 9/*metabolism
MH  - Middle Aged
MH  - Muscle, Smooth, Vascular/cytology/enzymology/*metabolism
MH  - Real-Time Polymerase Chain Reaction
MH  - Signal Transduction
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
EDAT- 2014/07/19 06:00
MHDA- 2015/04/14 06:00
CRDT- 2014/07/19 06:00
PHST- 2014/05/16 00:00 [accepted]
PHST- 2014/07/19 06:00 [entrez]
PHST- 2014/07/19 06:00 [pubmed]
PHST- 2015/04/14 06:00 [medline]
AID - 000362997 [pii]
AID - 10.1159/000362997 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2014;34(2):266-76. doi: 10.1159/000362997. Epub 2014 Jul 8.