Published January 2, 2008; doi:10. 0193-1849/08 $8.Versions of this Article: 294/3/E589 _most recent_ Services Google Scholar PubMed RNA SUPPRESSION OF ERK2 LEADS TO COLLAPSE OF MITOCHONDRIAL MEMBRANE POTENTIAL WITH ACUTE OXIDATIVE STRESS IN HUMAN LENS EPITHELIAL CELLS JAMES M.DEBORAH A.DAVID E.MARGARET H.PATRICK R._ 1Department of Cell Biology and Genetics, University of North Texas Health Science Center, Fort Worth, Texas; and 2Center for Cell Signaling and the Department of Microbiology, University of Virginia, School of Medicine, Charlottesville, Virginia _ Submitted 1 November 2007 ; accepted in final form 28 December 2007 17-Estradiol (E2) reduces oxidative stress-induced depolarization of mitochondrial membrane potential (MMP) in cultured human lens epithelial cells (HLE-B3).Mechanism by which the nongenomic effects of E2 contributed to the protection against mitochondrial membrane depolarization was investigated.Membrane integrity is regulated by phosphorylation of BAD, and it is known that phosphorylation of Ser112 inactivates BAD and prevents its participation in the mitochondrial death pathway.Found that E2 rapidly increased both the phosphorylation of ERK2 and Ser112 in BAD.Phosphorylated by p90 ribosomal S6 kinase (RSK), a Ser/Thr kinase, which is a downstream effector of ERK1/2.Of RSK by the RSK-specific inhibitor SL0101 did not reduce the level of E2-induced phosphorylation of Ser112.BAD using small interfering RNA did not alter mitochondrial membrane depolarization elicited by peroxide insult.Under the same conditions, silencing ERK2 dramatically increased membrane depolarizationpared with the control small interfering RNA.ERK2, functioning through a BAD-independent mechanism regulates MMP in humans lens epithelial cells.Propose that estrogen-induced activation of ERK2 acts to protect cells from acute oxidative stress.Despite the fact that ERK2 plays a regulatory role in mitochondrial membrane potential, estrogen was found to block mitochondrial membrane depolarization via an ERK-independent mechanism.17-estradiol; mitochondrial membrane potential; mitochondrial permeability transition Address for reprint requests and other correspondence: P.Dept.Cell Biology and Genetics, Univ.Read more Major policy issue lies behind odac's avastin decision
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