The ASK1-Signalosome regulates p38 MAPK activity in response to levels of endogenous oxidative stress in the Klotho mouse models of aging
Reactive oxygen species (ROS) and elevated levels of p38 MAPK activity accelerate physiological aging. This emphasizes the importance of understanding the molecular mechanism(s) that link ROS production to activation of the p38 mediated promotion of aging, longevity, and resistance to oxidative stre...
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Published in | Aging (Albany, NY.) Vol. 2; no. 9; pp. 597 - 611 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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15.09.2010
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Abstract | Reactive oxygen species (ROS) and elevated levels of p38 MAPK activity accelerate physiological aging. This emphasizes the importance of understanding the molecular mechanism(s) that link ROS production to activation of the p38 mediated promotion of aging, longevity, and resistance to oxidative stress. We examined Klotho(-/-) (elevated ROS) and Klotho overexpressing mice (low ROS and resistance to ROS) to determine whether the ROS-sensitive apoptosis signal-regulating kinase (ASK1)-signalosome -> p38 MAPK pathway plays a role in the accelerated aging of Klotho(-/-), and resistance to oxidative stress and extended lifespan in the Klotho overexpressing models. Our results suggest that increased endogenous ROS generated by Klotho(-/-) and resistance to oxidative stress in Klotho overexpression are linked to the regulation of ASK1-signalosome -> p38 activity. We propose that (a) the ASK1-signalosome -> p38 MAPK pathway is activated by oxidative stress due to ablation of the Klotho gene; (b) increased longevity by Klotho overexpression is linked to suppression of the ASK1-signalosome-p38 MAPK activity; (c) the ROS-responsive ASK1-signalosome regulates physiological aging via its regulation of p38 MAPK, through a mechanism that balances the levels of inhibitory vs. activating ASK1-signalosomes. We conclude that the Klotho suppressor-of-aging activity is linked to the ASK1-signalsome, a physiological ROS-sensitive signaling center. |
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AbstractList | Reactive oxygen species (ROS) and elevated levels of p38 MAPK activity accelerate physiological aging. This emphasizes the importance of understanding the molecular mechanism(s) that link ROS production to activation of the p38 mediated promotion of aging, longevity, and resistance to oxidative stress. We examinedKlotho
(-/-)
(elevated ROS) and Klotho overexpressing mice (low ROS and resistance to ROS) to determine whether the ROS-sensitive apoptosis signal-regulating kinase (ASK1)-signalosome → p38 MAPK pathway plays a role in the accelerated aging of Klotho
(-/-)
, and resistance to oxidative stress and extended lifespan in the Klotho overexpressing models. Our results suggest that increased endogenous ROS generated by Klotho
(-/-)
and resistance to oxidative stress in Klotho overexpression are linked to the regulation of ASK1-signalosome → p38 activity. We propose that (a) the ASK1-signalosome → p38 MAPK pathway is activated by oxidative stress due to ablation of the Klotho gene; (b) increased longevity by Klotho overexpression is linked to to suppression of the ASK1-signalosome-p38 MAPK activity; (c) the ROS-responsive ASK1-signalosome regulates physiological aging via its regulation of p38 MAPK, through a mechanism that balances the levels of inhibitory vs. activating ASK1-signalosomes. We conclude that the Klotho suppressor-of-aging activity is linked to the ASK1-signalsome, a physiological ROS-sensitive signaling center. Reactive oxygen species (ROS) and elevated levels of p38 MAPK activity accelerate physiological aging. This emphasizes the importance of understanding the molecular mechanism(s) that link ROS production to activation of the p38 mediated promotion of aging, longevity, and resistance to oxidative stress. We examined Klotho(-/-) (elevated ROS) and Klotho overexpressing mice (low ROS and resistance to ROS) to determine whether the ROS-sensitive apoptosis signal-regulating kinase (ASK1)-signalosome -> p38 MAPK pathway plays a role in the accelerated aging of Klotho(-/-), and resistance to oxidative stress and extended lifespan in the Klotho overexpressing models. Our results suggest that increased endogenous ROS generated by Klotho(-/-) and resistance to oxidative stress in Klotho overexpression are linked to the regulation of ASK1-signalosome -> p38 activity. We propose that (a) the ASK1-signalosome -> p38 MAPK pathway is activated by oxidative stress due to ablation of the Klotho gene; (b) increased longevity by Klotho overexpression is linked to suppression of the ASK1-signalosome-p38 MAPK activity; (c) the ROS-responsive ASK1-signalosome regulates physiological aging via its regulation of p38 MAPK, through a mechanism that balances the levels of inhibitory vs. activating ASK1-signalosomes. We conclude that the Klotho suppressor-of-aging activity is linked to the ASK1-signalsome, a physiological ROS-sensitive signaling center. |
Author | Papaconstantinou, John Hsieh, C-C Brobey, Reynolds Rosenblatt, Kevin P Kuro-o, Makoto |
AuthorAffiliation | 2 Department of Pathology, the University of Texas Southwestern Medical Center, Dallas, TX 75390, USA 1 Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA 3 The Brown Foundation Institute of Molecular Medicine, the University of Texas Health Science Center, Houston, TX 77030, USA |
AuthorAffiliation_xml | – name: 2 Department of Pathology, the University of Texas Southwestern Medical Center, Dallas, TX 75390, USA – name: 1 Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA – name: 3 The Brown Foundation Institute of Molecular Medicine, the University of Texas Health Science Center, Houston, TX 77030, USA |
Author_xml | – sequence: 1 givenname: C-C surname: Hsieh fullname: Hsieh, C-C organization: Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA – sequence: 2 givenname: Makoto surname: Kuro-o fullname: Kuro-o, Makoto – sequence: 3 givenname: Kevin P surname: Rosenblatt fullname: Rosenblatt, Kevin P – sequence: 4 givenname: Reynolds surname: Brobey fullname: Brobey, Reynolds – sequence: 5 givenname: John surname: Papaconstantinou fullname: Papaconstantinou, John |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20844314$$D View this record in MEDLINE/PubMed |
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Snippet | Reactive oxygen species (ROS) and elevated levels of p38 MAPK activity accelerate physiological aging. This emphasizes the importance of understanding the... |
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SubjectTerms | 14-3-3 Proteins - physiology Aging - physiology Animals Glucuronidase - genetics Glucuronidase - physiology Longevity - physiology MAP Kinase Kinase 3 - physiology MAP Kinase Kinase 6 - physiology MAP Kinase Kinase Kinase 5 - physiology Mice Mice, Knockout Models, Animal NF-E2-Related Factor 2 - physiology Oxidative Stress - physiology p38 Mitogen-Activated Protein Kinases - physiology Reactive Oxygen Species - metabolism Research Paper Signal Transduction - physiology Thioredoxins - physiology |
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Title | The ASK1-Signalosome regulates p38 MAPK activity in response to levels of endogenous oxidative stress in the Klotho mouse models of aging |
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