PMID- 7589574
OWN - NLM
STAT- MEDLINE
DCOM- 19951219
LR  - 20190621
IS  - 0014-5793 (Print)
IS  - 0014-5793 (Linking)
VI  - 374
IP  - 3
DP  - 1995 Nov 6
TI  - Synergistic induction of monocyte chemoattractant protein-1 (MCP-1) by 
      platelet-derived growth factor and interleukin-1.
PG  - 375-8
AB  - Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the 
      recruitment of monocytic cells to the site of inflammation. Resting mesangial 
      cells express barely detectable levels of MCP-1 mRNA. Treatment of rat mesangial 
      cells with platelet products PDGF-AB, PDGF-BB or serotonin transiently induced 
      MCP-1 expression with a maximum after 2 to 4 h and a decline to baseline after 6 
      to 8 h. Different kinetics were observed with interleukin-1 beta (IL-1 beta), 
      which induced a long lasting elevation of MCP-1 mRNA for more than 20 h. 
      Together, PDGF and IL-1 beta synergistically induced MCP-1 expression. The effect 
      was most obvious after 16 to 20 h, when induction by PDGF alone had already 
      faded, but still PDGF strongly enhanced IL-1 beta-induced MCP-1 mRNA expression. 
      MCP-1 mRNA levels were regulated by changes in the stability of the mRNA: 
      inhibition of protein synthesis by cycloheximide by itself induced MCP-1 mRNA 
      expression and led to superinduction in the presence of PDGF. Message 
      stabilization also contributed to the synergistic action of PDGF and IL-1 beta: 
      the apparent half life of MCP-1 mRNA determined in the presence of actinomycin D 
      was prolonged when both stimuli were added together. We could thus show that in 
      mesangial cells different types of cytokines and growth factors synergize to 
      enhance MCP-1, the secretion of which could lead to the recruitment of monocytic 
      cells into the inflamed mesangium.
FAU - Goppelt-Struebe, M
AU  - Goppelt-Struebe M
AD  - Medizinische Klinik IV, Universitat Erlangen-Nurnberg, Germany.
FAU - Stroebel, M
AU  - Stroebel M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - FEBS Lett
JT  - FEBS letters
JID - 0155157
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1CC1JFE158 (Dactinomycin)
RN  - 333DO1RDJY (Serotonin)
RN  - 98600C0908 (Cycloheximide)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Cycloheximide/pharmacology
MH  - Dactinomycin/pharmacology
MH  - Drug Stability
MH  - Drug Synergism
MH  - Gene Expression/*drug effects
MH  - Glomerular Mesangium/metabolism
MH  - Half-Life
MH  - Interleukin-1/*pharmacology
MH  - Kinetics
MH  - Platelet-Derived Growth Factor/*pharmacology
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Serotonin/pharmacology
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1995/11/06 00:00
MHDA- 1995/11/06 00:01
CRDT- 1995/11/06 00:00
PHST- 1995/11/06 00:00 [pubmed]
PHST- 1995/11/06 00:01 [medline]
PHST- 1995/11/06 00:00 [entrez]
AID - 0014-5793(95)01155-8 [pii]
AID - 10.1016/0014-5793(95)01155-8 [doi]
PST - ppublish
SO  - FEBS Lett. 1995 Nov 6;374(3):375-8. doi: 10.1016/0014-5793(95)01155-8.