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Estrogens modulate bovine vascular endothelial cell permeability and HSP 25 expression concomitantly
F Delarue1, S Daunes, R Elhage
1Institut National de la Santé et de la Recherche Médicale Unité 397, Institut L. Bugnard, Centre Hospitalier Universitaire (CHU) Rangueil, 31403 Toulouse Cedex 4, France.
The American Journal of Physiology
|September 2, 1998
Summary
Estrogens regulate endothelial permeability and low-density lipoprotein transport by influencing heat shock protein 25 (HSP 25) expression. This finding sheds light on the mechanisms behind estrogens' atheroprotective effects.
Area of Science:
- Endocrinology
- Vascular Biology
- Cell Biology
Background:
- Estrogens exhibit atheroprotective properties, observed in postmenopausal women undergoing hormone replacement therapy.
- The precise mechanisms underlying estrogen's vascular effects, particularly on endothelial permeability, remain largely unelucidated.
- Estrogens are hypothesized to modulate endothelial barrier function against atherogenic lipoproteins.
Purpose of the Study:
- To investigate the role of estrogens in regulating endothelial permeability and lipoprotein transport.
- To explore the cellular mechanisms, including protein expression, involved in estrogen-mediated endothelial barrier modulation.
- To utilize an in vitro model to dissect the relationship between estrogen concentration and macromolecular transport.
Main Methods:
- Employing bovine vascular endothelial cells as an in vitro model system.
- Quantifying low-density lipoprotein transport across the endothelial monolayer.
- Measuring macromolecular transport as a function of estrogen concentration.
- Assessing the expression of heat shock protein 25 (HSP 25) in response to estrogen treatment.
Main Results:
- Estrogens significantly regulated low-density lipoprotein transport and endothelial monolayer permeability.
- Macromolecular transport demonstrated a second-order polynomial relationship with estrogen concentration.
- Estrogen-induced regulation of permeability was strongly correlated with increased expression of HSP 25.
- HSP 25's known roles in pinocytosis and cytoskeleton remodeling suggest its involvement in this process.
Conclusions:
- Estrogens modulate endothelial permeability and lipoprotein transport through mechanisms involving HSP 25.
- HSP 25 plays a crucial role in the estrogenic control of transcellular permeability in endothelial monolayers.
- These findings provide mechanistic insights into the atheroprotective effects of estrogens.