PMID- 10479651
OWN - NLM
STAT- MEDLINE
DCOM- 19991007
LR  - 20190831
IS  - 1079-5642 (Print)
IS  - 1079-5642 (Linking)
VI  - 19
IP  - 9
DP  - 1999 Sep
TI  - 9-cis retinoic acid induces monocyte chemoattractant protein-1 secretion in human 
      monocytic THP-1 cells.
PG  - 2105-11
AB  - Monocyte migration and activation are regulated by monocyte chemoattractant 
      protein-1 (MCP-1). Prior studies have shown MCP-1 expression is modulated by a 
      variety of ligands that act through extracellular receptors. In the current 
      study, we show 9-cis retinoic acid (RA), a ligand for the nuclear hormone 
      receptor retinoid X receptor (RXR) and retinoic acid receptor (RAR), markedly 
      induces the expression of MCP-1. In human THP-1 monocytic leukemia cells cultured 
      with RA (0.05 to 500 nmol/L), MCP-1 expression was induced rapidly, 
      significantly, and dose-dependently by as much as 165-fold. MCP-1 RNA level was 
      also increased in RA-treated cells. Expression of PPARgamma, a heterodimer 
      partner of RXR, is also markedly induced by RA in THP-1 cells. However, BRL49653, 
      a PPARgamma ligand, failed to induce MCP-1 secretion either alone or to modify 
      the expression level induced by RA. In contrast, BRL49653 significantly increased 
      MCP-1 (biotinylated MCP-1) binding to THP-1 cells, whereas RA had no effect. 
      Other peroxisome proliferator activated receptor (PPAR) ligands, 15d-PGJ(2) and 
      troglitazone (PPARgamma), Wy14,643 (PPARalpha), and PD195599 (PPARbeta) inhibited 
      the induction of MCP-1 by RA. RA's effect on MCP-1 expression in human elutriated 
      monocytes were similar to that observed in the THP-1 cells. These studies 
      identify RA as a nuclear signal for MCP-1 induction in undifferentiated human 
      monocytic cells. These studies also suggest monocyte MCP-1 expression induced 
      through RA may modulate cell migration.
FAU - Zhu, L
AU  - Zhu L
AD  - Department of Vascular and Cardiac Diseases Parke-Davis Pharmaceutical Research, 
      Ann Arbor, Michigan, USA.
FAU - Bisgaier, C L
AU  - Bisgaier CL
FAU - Aviram, M
AU  - Aviram M
FAU - Newton, R S
AU  - Newton RS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Thiazoles)
RN  - 0 (Thiazolidinediones)
RN  - 0 (Transcription Factors)
RN  - 05V02F2KDG (Rosiglitazone)
RN  - 1UA8E65KDZ (Alitretinoin)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Alitretinoin
MH  - Blood Cells/drug effects/metabolism
MH  - Chemokine CCL2/antagonists & inhibitors/genetics/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - Monocytes/*drug effects/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Receptors, Cytoplasmic and Nuclear/metabolism
MH  - Rosiglitazone
MH  - Signal Transduction/physiology
MH  - Thiazoles/pharmacology
MH  - *Thiazolidinediones
MH  - Transcription Factors/metabolism
MH  - Tretinoin/*pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1999/09/10 00:00
MHDA- 1999/09/10 00:01
CRDT- 1999/09/10 00:00
PHST- 1999/09/10 00:00 [pubmed]
PHST- 1999/09/10 00:01 [medline]
PHST- 1999/09/10 00:00 [entrez]
AID - 10.1161/01.atv.19.9.2105 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 1999 Sep;19(9):2105-11. doi: 
      10.1161/01.atv.19.9.2105.