Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1908588 | Free Radical Biology and Medicine | 2012 | 12 Pages |
Abstract
⸠ER stress in retinal pigment epithelium (RPE) leads to mitochondrial dysfunction. ⸠ER stress in RPE results in apoptosis from activation of caspasesâ4 and â3. ⸠ER stress-mediated apoptosis in RPE involves PERK-eIf2α, ATF6, and CHOP. ⸠αB Crystallin deficiency in RPE augments ER stress-induced apoptosis. ⸠αB Crystallin overexpression protects RPE from ER stress-induced apoptosis.
Keywords
RPEαB CrystallintunicamycinBFAThapsigarginUPRMPTAMDGSHROSEndoplasmic reticulum (ER) stressmitochondrial permeability transitionretinal pigment epitheliumRetinal pigment epithelium (RPE)brefeldinApoptosisage-related macular degenerationendoplasmic reticulumMitochondriaUnfolded protein responseGlutathioneReactive oxygen species
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Authors
Guorui Dou, Parameswaran G. Sreekumar, Christine Spee, Shikun He, Stephen J. Ryan, Ram Kannan, David R. Hinton,