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Estradiol suppresses MCP-1 expression In vivo : implications for atherosclerosis
S Pervin1, R Singh, M E Rosenfeld
1Department 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.
Arteriosclerosis, Thrombosis, and Vascular Biology
|October 9, 1998
Summary
Estradiol, a key hormone, reduces monocyte chemoattractant protein-1 (MCP-1) in rabbits, mitigating a crucial step in atherosclerosis development. This finding highlights estradiol
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Immunology
Background:
- Atherosclerosis involves monocyte adhesion and migration into artery walls.
- Monocyte chemoattractant protein-1 (MCP-1) is a key chemokine driving this process.
- The role of 17beta-estradiol in preventing atherosclerosis is not fully understood.
Purpose of the Study:
- To investigate the in vivo effects of estradiol on MCP-1 protein and mRNA expression in rabbits.
- To determine if estradiol modulates MCP-1 levels during hypercholesterolemia.
Main Methods:
- Rabbits were fed a cholesterol-enriched or normal diet for 6 weeks.
- Estradiol supplementation was administered to ovariectomized rabbits.
- MCP-1 protein and mRNA levels were quantified using Western blot, chemotaxis bioassays, and RT-PCR.
Main Results:
- High-cholesterol diet significantly increased MCP-1 protein and mRNA in aorta.
- Estradiol supplementation attenuated these cholesterol-induced increases in MCP-1.
- Estradiol also prevented elevated MCP-1 levels in normocholesterolemic ovariectomized rabbits.
Conclusions:
- Physiological concentrations of estradiol modulate both basal and hypercholesterolemia-induced MCP-1 protein levels.
- Estradiol may retard atherogenesis by inhibiting MCP-1 expression and subsequent monocyte migration.