PMID- 9763529
OWN - NLM
STAT- MEDLINE
DCOM- 19981102
LR  - 20190831
IS  - 1079-5642 (Print)
IS  - 1079-5642 (Linking)
VI  - 18
IP  - 10
DP  - 1998 Oct
TI  - Estradiol suppresses MCP-1 expression In vivo : implications for atherosclerosis.
PG  - 1575-82
AB  - The mechanisms by which 17beta-estradiol retards atherogenesis are not known. The 
      adhesion of monocytes to endothelial cells followed by the migration of monocytes 
      into the artery wall are key cellular events that occur throughout the entire 
      atherogenic process and may be responsive to estradiol. Monocyte chemoattractant 
      protein-1 (MCP-1), a chemokine that is expressed in atherosclerotic lesions, is 
      thought to play a major role in stimulating the migration of blood monocytes into 
      developing atherosclerotic lesions. We therefore assessed the effects of 
      estradiol in vivo on MCP-1 protein and mRNA expression in the descending thoracic 
      aorta of rabbits fed a cholesterol-enriched (0.5%) diet for 6 weeks and in 
      animals fed normal chow. MCP-1 protein was quantified by Western blot analysis 
      and monocyte chemotaxis bioassay, and reverse transcription-polymerase chain 
      reaction was used to ascertain the level of MCP-1 mRNA expression. We observed 
      that in both ovary-intact and ovariectomized (OVX) animals, MCP-1 protein and 
      mRNA expression were significantly increased by 6 weeks in animals fed a 
      high-cholesterol diet. The cholesterol-induced increase in MCP-1 protein and mRNA 
      expression was significantly attenuated in OVX rabbits supplemented with 
      estradiol pellets (1.5- and 10.0-mg 60-day-release pellets), which yielded a 
      range of estradiol concentrations encompassing the physiological levels. MCP-1 
      protein and mRNA expression were increased in normocholesterolemic OVX rabbits 
      compared with normocholesterolemic ovary-intact animals, and this increase was 
      prevented in OVX animals supplemented with estradiol pellets. Our observations 
      indicate that both basal and hypercholesterolemia-induced increases in MCP-1 
      protein are modulated by physiological concentrations of estradiol.
FAU - Pervin, S
AU  - Pervin S
AD  - Department of Obstetrics and Gynecology, the Department of Molecular and Medical 
      Pharmacology, and the Department of Internal Medicine, UCLA School of Medicine, 
      University of California, Los Angeles, USA.
FAU - Singh, R
AU  - Singh R
FAU - Rosenfeld, M E
AU  - Rosenfeld ME
FAU - Navab, M
AU  - Navab M
FAU - Chaudhuri, G
AU  - Chaudhuri G
FAU - Nathan, L
AU  - Nathan L
LA  - eng
GR  - HD-31467/HD/NICHD NIH HHS/United States
GR  - HL-46843/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cholesterol, Dietary)
RN  - 0 (RNA, Messenger)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/*etiology/metabolism
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cholesterol, Dietary/metabolism
MH  - Estradiol/administration & dosage/*metabolism
MH  - Female
MH  - Gene Expression
MH  - Ovariectomy
MH  - Ovary
MH  - RNA, Messenger
MH  - Rabbits
EDAT- 1998/10/09 00:00
MHDA- 1998/10/09 00:01
CRDT- 1998/10/09 00:00
PHST- 1998/10/09 00:00 [pubmed]
PHST- 1998/10/09 00:01 [medline]
PHST- 1998/10/09 00:00 [entrez]
AID - 10.1161/01.atv.18.10.1575 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 1998 Oct;18(10):1575-82. doi: 
      10.1161/01.atv.18.10.1575.