Mitochondrial translocation of estrogen receptor β affords resistance to oxidative insult-induced apoptosis and contributes to the pathogenesis of endometriosis

Liao TL, Tien-Ling Liao, Yu‐Ching Lee, Yu-Ching Lee, Lee YC, Chii-Ruey Tzeng, Chii‐Ruey Tzeng, Tzeng CR, Wang YP, Yi-Pei Wang, Heng‐Yu Chang, Heng-Yu Chang, Chang HY, Yung‐Feng Lin, Lin YF, Yung-Feng Lin, Shu-Huei Kao, Shu‐Huei Kao
Free radical biology & medicine · 2019 · vol. 134 , pp. 359–373 · doi:10.1016/j.freeradbiomed.2019.01.022 · PMID:30684560 · W2914087220
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Estrogen receptor beta translocates to mitochondria, protecting against oxidative stress-induced apoptosis and contributing to endometriosis development.

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Abstract

Endometriosis is the major cause of female infertility and has been linked to the action of estrogen and estrogen receptor (ER). A new pool of ERβ locates within mitochondria, which regulates the endometriotic cell withstanding external insults, but its effect remains controversial. We hypothesize that mitochondrial estrogen receptor ERβ (mtERβ) is a pivotal regulator in estradiol-mediated cell protection leading to the endometriotic progression. We observed elevated levels of ERβ in the endometriotic tissues. A dramatic increase of ERβ in mitochondria (mtERβ) was found in the ectopic endometriotic tissues, or the estradiol-primed primary endometriotic cells. We analyzed the mtERβ-specific overexpressing clone (mtsERβ), which exhibited higher mitochondrial bioenergetics and lower reactive oxygen species (ROS) generation. The mtsERβ-overexpressed endometriotic cells displayed an enhanced migration phenotype, whereas significantly attenuated migration by mitochondrial respiratory inhibitor (oligomycin) or ERβ deficiency by shERβ. Further investigations revealed that ERβ directly modulated mitochondrial DNA (mtDNA) gene expression by interacting with mtDNA D-loop and polymerase γ. The mtsERβ afforded a resistance to oxidative insult-induced apoptosis through the induction of the ROS scavenger enzyme Mn-superoxide dismutase and anti-apoptotic protein Bcl-2. Collectively, the demonstration of mtERβ responses in restoration of mitochondrial bioenergetics and inhibition of mitochondria-dependent apoptotic events provides insight into the pathogenesis of endometriosis, suggesting ERβ-selective estrogen receptor modulator may serve as novel therapeutics of endometriosis in the future.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Endometriosis Estrogen Receptor beta Mitochondria Oxidative Stress Reactive Oxygen Species Endometriosis Endometriosis Energy Metabolism Estrogen Receptor beta Female Humans Mitochondria Mitochondria Mitochondrial Dynamics Organelle Biogenesis Protein Transport Reactive Oxygen Species

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