PMID- 10381273
OWN - NLM
STAT- MEDLINE
DCOM- 19990811
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 144
IP  - 1
DP  - 1999 May
TI  - Expression of monocyte chemoattractant protein-1 cDNA in vascular smooth muscle 
      cells: induction of the synthetic phenotype: a possible clue to SMC 
      differentiation in the process of atherogenesis.
PG  - 15-23
AB  - In the arterial wall, smooth muscle cells (SMC) normally exist in a quiescent, 
      differentiated state, representing the contractile phenotype. During the 
      development of atherosclerosis SMC change towards the synthetic phenotype going 
      along with proliferation, chemotactic response and increased monocyte binding. 
      Expression of monocyte chemoattractant protein-1 (MCP-1), a potent 
      chemoattractant for monocytes, has been shown to be among the earliest events in 
      atherogenesis. We investigated the effect of MCP-1 on differentiated and 
      dedifferentiated SMC. Differentiation of SMC was induced using Matrigel as a 
      matrix for cultivation. MCP-1 was expressed in SMC by means of a recombinant 
      adenovirus. Expression of MCP-1 led to dedifferentiation of SMC as demonstrated 
      by induction of cytokeratin 18, a marker for the synthetic phenotype. 
      Concurrently, migration was only detectable in MCP-1 expressing cells, whereas 
      SMC infected with a control virus, coding for the nuclear-targeted lacZ gene 
      showed no migration. The expression of intercellular adhesion molecule-1 (ICAM-1) 
      could be demonstrated in synthetic SMC and was induced after infection of 
      differentiated cells with recombinant adenovirus, coding for MCP-1 (AdMCP-1). 
      Expression of ICAM-1 was associated with a tenfold higher monocyte binding 
      compared to lacZ infected cells. Our data suggest that MCP-1 plays an important 
      role for SMC in the functional switch from the contractile to the synthetic 
      phenotype in the course of atherogenesis.
FAU - Denger, S
AU  - Denger S
AD  - Department of Cardiology, University of Heidelberg, Germany.
FAU - Jahn, L
AU  - Jahn L
FAU - Wende, P
AU  - Wende P
FAU - Watson, L
AU  - Watson L
FAU - Gerber, S H
AU  - Gerber SH
FAU - Kubler, W
AU  - Kubler W
FAU - Kreuzer, J
AU  - Kreuzer J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA, Complementary)
RN  - 0 (Genetic Markers)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 68238-35-7 (Keratins)
SB  - IM
MH  - Adenoviridae
MH  - Arteriosclerosis/pathology/*physiopathology/virology
MH  - Base Sequence
MH  - Cell Adhesion
MH  - Cell Culture Techniques
MH  - Cell Differentiation/genetics/physiology
MH  - Chemokine CCL2/*genetics
MH  - DNA, Complementary/*analysis
MH  - Gene Expression Regulation/physiology
MH  - Genetic Markers
MH  - Humans
MH  - Immunoblotting
MH  - Immunohistochemistry
MH  - Intercellular Adhesion Molecule-1/analysis
MH  - Keratins/analysis
MH  - Molecular Sequence Data
MH  - Monocytes/metabolism
MH  - Muscle, Smooth, Vascular/*chemistry/virology
MH  - Phenotype
MH  - Polymerase Chain Reaction
MH  - Sensitivity and Specificity
EDAT- 1999/06/25 00:00
MHDA- 1999/06/25 00:01
CRDT- 1999/06/25 00:00
PHST- 1999/06/25 00:00 [pubmed]
PHST- 1999/06/25 00:01 [medline]
PHST- 1999/06/25 00:00 [entrez]
AID - S0021-9150(99)80054-9 [pii]
AID - 10.1016/s0021-9150(99)00033-7 [doi]
PST - ppublish
SO  - Atherosclerosis. 1999 May;144(1):15-23. doi: 10.1016/s0021-9150(99)00033-7.