Abstract
Background Previous work from our laboratory demonstrated the involvement of “intrinsic” mitochondrial apoptotic signaling in vascular hyperpermeability. The objective of this study was to determine if 17β-estradiol, a known inhibitor of apoptosis, would attenuate microvascular endothelial cell hyperpermeability. Methods Rat lung microvascular endothelial cell monolayers were treated with 17β-estradiol or estrogen-receptor antagonist ICI 182780 after transfection with BAK peptide (5 μg/mL). Fluorescein isothiocyanate (FITC)–albumin was used to determine the change in permeability. Mitochondrial reactive oxygen species (ROS) formation and transmembrane potential were determined using 123 dihydrorhodamine and JC-1, respectively. Cytosolic cytochrome c levels and caspase-3 activity were determined using enzyme-linked immunosorbent assay and fluorometric assay respectively. Results 17β-estradiol (10 n m) attenuated BAK-induced hyperpermeability ( P < .05), ROS formation, cytochrome c release, and caspase-3 activation. The estrogen receptor antagonist ICI 182780 blocked the protective effect of 17β-estradiol on hyperpermeability ( P < .05). Conclusions 17β-estradiol attenuates BAK-induced hyperpermeability in rat lung microvascular endothelial cells by way of an estrogen-receptor mediated pathway.
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