PMID- 12845752
OWN - NLM
STAT- MEDLINE
DCOM- 20031216
LR  - 20240202
IS  - 0257-716X (Print)
IS  - 0257-716X (Linking)
VI  - 20
IP  - 1
DP  - 2000
TI  - Interleukin-1 beta, tumor necrosis factor-alpha and lipopolysaccharide induce 
      expression of monocyte chemoattractant protein-1 in calf aortic smooth muscle 
      cells.
PG  - 36-8
AB  - To investigate whether interleukin-1 beta(IL-1 beta), tumor necrosis factor-alpha 
      (TNF-alpha) and lipopolysaccharide (LPS) induce expression of monocyte 
      chemoattractant protein-1 (MCP-1) mRNA and protein in calf aortic smooth muscle 
      cells(SMCs), calf aortic SMCs were cultured by a substrate-attached explant 
      method. The cultured SMCs were used between the third to the fifth passage. After 
      the cells became confluent, the SMCs were exposed to 2 ng/ml IL-1 beta, 20 ng/ml 
      TNF-1 alpha and 100 ng/ml LPS respectively, and the total RNA of SMCs which were 
      incubated for 4 h at 37 degrees C were extracted from the cells by using 
      guanidinium isothiocyanate method. The expression of MCP-1 mRNA in SMCs was 
      detected by using dot blotting analysis using a probe of gamma-32P-end-labelled 
      35-mer oligonucleotide. After a 24-h incubation, the media conditioned by the 
      cultured SMCs were collected. The MCP-1 protein content in the conditioned media 
      was determined by using sandwich ELISA. The results were as follows: Dot blotting 
      analysis showed that the cultured SMCs could express MCP-1 mRNA. After a 4-h 
      exposure to IL-1 beta, TNF-alpha and LPS, the MCP-1 mRNA expression in SMCs was 
      increased (3.6-fold, 2.3-fold and 1.6-fold, respectively). ELISA showed that the 
      levels of MCP-1 protein in the conditioned media were also increased (2.9-fold, 
      1.7-fold and 1.1-fold, respectively). The results suggest that calf aortic SMCs 
      could express MCP-1 mRNA and protein. IL-1 beta and TNF-alpha can induce strong 
      expression of MCP-1 mRNA and protein, and the former is more effective than the 
      latter.
FAU - Meng, F
AU  - Meng F
AD  - Department of Pathology, School of Basic Medical Sciences, Tongji Medical 
      University, Wuhan 430030.
FAU - Deng, Z
AU  - Deng Z
FAU - Ni, J
AU  - Ni J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - J Tongji Med Univ
JT  - Journal of Tongji Medical University = Tong ji yi ke da xue xue bao
JID - 8605495
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Aorta/metabolism
MH  - Cattle
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Interleukin-1/*pharmacology
MH  - Lipopolysaccharides/*pharmacology
MH  - Muscle, Smooth, Vascular/cytology/*metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2003/07/09 05:00
MHDA- 2003/12/17 05:00
CRDT- 2003/07/09 05:00
PHST- 2003/07/09 05:00 [pubmed]
PHST- 2003/12/17 05:00 [medline]
PHST- 2003/07/09 05:00 [entrez]
AID - 10.1007/BF02887671 [doi]
PST - ppublish
SO  - J Tongji Med Univ. 2000;20(1):36-8. doi: 10.1007/BF02887671.