Cavinato 2016 Abstract Mito Xmas Meeting Innsbruck

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Involvement of mitophagy in the elimination of damaged mitochondria during the process of UVB-induced senescence.

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Cavinato M, Koziel R, Jenewein B, Hermann M, Romani N, Jansen-Duerr P (2016)

Event: Mito Xmas Meeting 2016 Innsbruck AT

Skin aging is the result of two types of aging, “intrinsic aging” an inevitable consequence of physiologic and genetic determined changes and “extrinsic aging” which is dependent on external factors like exposure to sunlight, smoking, dietary habits among others. UV and other forms of ionizing radiation cause skin injury through the generation of free radicals and other oxidative byproducts as well as DNA damage. The oxidized proteins are generally degraded by the ubiquitin-proteasome system or by autophagy, and alterations on these pathways lead to accumulation of damaged molecules. The activity of proteasomes and autophagic organelles is regulated by overlapping signals, and regulatory cross-talk between both quality control systems has been described. Likewise, excessive ROS production leads to impairment of mitochondria with consequences that are related to several age-related diseases as well as to the physiology of normal aging. We have previously demonstrated that inhibition of proteasomal degradation of damaged proteins and activation of autophagosome formation are early events in UVB-induced senescence of human dermal fibroblasts (HDF), dependent on UVB-induced accumulation of reactive oxygen species (ROS). Here we show that UVB treatment of HDFs leads to impaired mitochondrial function, damage to mitochondrial structure and disruption of mitochondrial network and that these damaged organelles are eliminated by mitophagy. Under these conditions, mitophagy receptor Bnip3L/Nix is differentially regulated in fibroblasts. Elimination of Bnip3L/Nix increases cell proliferation and inhibits mitophagy activation upon UVB treatment. These findings have potential implications for fundamental as well as translational research into skin aging, and in particular photoaging.


O2k-Network Lab: AT Innsbruck Jansen-Duerr P


Labels: Pathology: Aging;senescence  Stress:Oxidative stress;RONS  Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell, Fibroblast 




Event: B1, Oral 


Affiliations

Cavinato M(1), Koziel R(1), Jenewein B(1), Hermann M(2), Romani N(3), Jansen-Dürr P(1)
  1. Inst Biomedical Aging Research, Univ Innsbruck, Austria
  2. Dept Anesthesiology Critical Care Medicine, Medical Univ Innsbruck, Austria
  3. Dept Dermatology Venerology, Medical Univ Innsbruck, Austria