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Published on: August 13, 2019
17beta-estradiol mediates protection against microvascular endothelial cell hyperpermeability
Binu Tharakan1, Robert Corprew, Felicia A Hunter
1Department of Surgery, College of Medicine, Texas A&M University Health Science Center, Temple, TX, USA.
American Journal of Surgery
|February 3, 2009
Summary
17beta-estradiol reduces vascular hyperpermeability by inhibiting apoptosis. This protective effect is mediated through estrogen receptors, suggesting a therapeutic role for 17beta-estradiol in vascular conditions.
Area of Science:
- Vascular Biology
- Mitochondrial Signaling
- Endocrinology
Background:
- Intrinsic mitochondrial apoptotic signaling contributes to vascular hyperpermeability.
- 17beta-estradiol is a known inhibitor of apoptosis.
Purpose of the Study:
- To investigate if 17beta-estradiol attenuates microvascular endothelial cell hyperpermeability.
- To elucidate the role of estrogen receptors in this process.
Main Methods:
- Rat lung microvascular endothelial cells were treated with 17beta-estradiol or ICI 182780 (estrogen receptor antagonist) after BAK peptide transfection.
- Permeability was assessed using FITC-albumin.
- Mitochondrial reactive oxygen species (ROS), transmembrane potential, cytosolic cytochrome c, and caspase-3 activity were measured.
Main Results:
- 17beta-estradiol significantly attenuated BAK-induced hyperpermeability, ROS formation, cytochrome c release, and caspase-3 activation.
- The estrogen receptor antagonist ICI 182780 blocked the protective effects of 17beta-estradiol.
- These findings indicate a role for estrogen receptors in mediating the protective effects.
Conclusions:
- 17beta-estradiol attenuates BAK-induced hyperpermeability in rat lung microvascular endothelial cells.
- This effect is mediated through an estrogen-receptor dependent pathway.
