This is not an easy read but does it not have some thought provoking implications? ( Which is why I have posted it here rather than in articles of interest)
Different balance alpha and beta and type of receptors and how do receptors compare with those in membrane.
Where is the key switching blocking re oestrogen denial taking place?
Preventing death of cells at mitochondrial level by oestrogen blocking (or may have nothing to do with it)? Has this got anything to do with the ways cells are protected for growing babies etc.
Could the existence of receptor on the membrane nucleous and mitochondria result in mixed oestrogen receptor status.
Intigueing through the thick fog.
RB
FULL ARTICLE
http://www.pubmedcentral.gov/article...medid=16495339
Functional Estrogen Receptors in the Mitochondria of Breast Cancer Cells
Ali Pedram,*â€* Mahnaz Razandi,*â€* Douglas C. Wallace,‡§ and Ellis R. Levin*‡∥
* Division of Endocrinology, Veterans Affairs Medical Center, Long Beach, Long Beach, CA 90822
â€* Department of Medicine, University of California, Irvine, Irvine CA 92717
‡ Department of Biochemistry, University of California, Irvine, Irvine CA 92717
∥ Department of Pharmacology, University of California, Irvine, Irvine CA 92717
§ Department of the Center for Molecular and Mitochondrial Medicine and Genetics, University of California, Irvine, Irvine CA 92717
Steroid hormones have been reported to indirectly impact mitochondrial functions, attributed to nuclear receptor-induced production of proteins that localize in this cytoplasmic organelle. Here we show high-affinity estrogen receptors in the mitochondria of MCF-7 breast cancer cells and endothelial cells, compatible with classical estrogen receptors ERα and ERβ. We report that in MCF-7, estrogen inhibits UV radiation-induced cytochrome C release, the decrease of the mitochondrial membrane potential, and apoptotic cell death. UV stimulated the formation of mitochondrial reactive oxygen species (mROS), and mROS were essential to inducing mitochondrial events of cell death. mROS mediated the UV activation of c-jun N-terminal kinase (JNK), and protein kinase C (PKC) δ, underlying the subsequent translocation of Bax to the mitochondria where oligomerization was promoted. E2 (estradiol) inhibited all these events, directly acting in mitochondria to inhibit mROS by rapidly up-regulating manganese superoxide dismutase activity. We implicate novel functions of ER in the mitochondria of breast cancer that lead to the survival of the tumor cells.
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