PMID- 7836768
OWN - NLM
STAT- MEDLINE
DCOM- 19950227
LR  - 20220408
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 154
IP  - 4
DP  - 1995 Feb 15
TI  - Estrogen modulation of JE/monocyte chemoattractant protein-1 mRNA expression in 
      murine macrophages.
PG  - 1838-45
AB  - The chemotactic cytokine, monocyte chemoattractant protein-1 (MCP-1), and its 
      murine homologue, JE, have been detected in atherosclerotic lesions but not in 
      normal arteries, implicating that these proinflammatory cytokines may be involved 
      in the pathogenesis of atherosclerosis. Epidemiologic studies reveal that 
      postmenopausal women receiving estrogen replacement for treatment of osteoporosis 
      have a greatly reduced risk of developing cardiovascular disease. Because 
      JE/MCP-1 and estrogen play regulatory roles in the development of atherosclerotic 
      lesions, we chose to examine the effect of estrogen treatment on JE/MCP-1 mRNA 
      expression in macrophages. 17 beta-estradiol (E2) inhibited LPS-stimulated 
      JE/MCP-1 mRNA expression in ANA-1 and J774A.1 murine macrophage cell lines and in 
      thioglycolate-elicited murine peritoneal macrophages. Inhibition of JE/MCP-1 mRNA 
      ranged from 50 to 90%, with a maximal effect occurring at a concentration of 300 
      pg/ml E2. Conversely, E2 had little effect on LPS-stimulated TNF-alpha mRNA 
      production. Treatment of LPS-stimulated macrophages with moxestrol, an estrogen 
      agonist, resulted in a similar inhibition, and the addition of the estrogen 
      antagonist, tamoxifen, reversed E2 inhibition of JE/MCP-1 mRNA expression. 
      Progesterone failed to inhibit LPS-induced JE/MCP-1 mRNA expression. 
      Immunohistochemical analysis revealed the presence of estrogen receptors in ANA-1 
      cells, indicating that E2 inhibition of LPS-induced JE/MCP-1 mRNA expression in 
      murine macrophages may be mediated through the estrogen receptor. Thus, another 
      mechanism whereby estrogen exerts antiatherogenic effects may be through 
      prevention of macrophage accumulation in the atherosclerotic lesion.
FAU - Frazier-Jessen, M R
AU  - Frazier-Jessen MR
AD  - Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, 
      Maywood, IL 60153.
FAU - Kovacs, E J
AU  - Kovacs EJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (RNA, Messenger)
RN  - 094ZI81Y45 (Tamoxifen)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
GS  - myc
GS  - raf
MH  - Animals
MH  - Arteriosclerosis/physiopathology/prevention & control
MH  - Cell Line
MH  - Cells, Cultured
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*biosynthesis/genetics
MH  - Estradiol/*pharmacology
MH  - Female
MH  - Gene Expression Regulation/*drug effects
MH  - Macrophages, Peritoneal/*drug effects/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Progesterone/pharmacology
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Sex Factors
MH  - Tamoxifen/pharmacology
EDAT- 1995/02/15 00:00
MHDA- 1995/02/15 00:01
CRDT- 1995/02/15 00:00
PHST- 1995/02/15 00:00 [pubmed]
PHST- 1995/02/15 00:01 [medline]
PHST- 1995/02/15 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1995 Feb 15;154(4):1838-45.