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10.1074/jbc.M112.445965

http://scihub22266oqcxt.onion/10.1074/jbc.M112.445965
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suck abstract from ncbi


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pmid23620592
      J+Biol+Chem 2013 ; 288 (24 ): 17214-24
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  • Wnt/?-catenin signaling protects mouse liver against oxidative stress-induced apoptosis through the inhibition of forkhead transcription factor FoxO3 #MMPMID23620592
  • Tao GZ ; Lehwald N ; Jang KY ; Baek J ; Xu B ; Omary MB ; Sylvester KG
  • J Biol Chem 2013[Jun]; 288 (24 ): 17214-24 PMID23620592 show ga
  • Numerous liver diseases are associated with extensive oxidative tissue damage. It is well established that Wnt/?-catenin signaling directs multiple hepatocellular processes, including development, proliferation, regeneration, nutrient homeostasis, and carcinogenesis. It remains unexplored whether Wnt/?-catenin signaling provides hepatocyte protection against hepatotoxin-induced apoptosis. Conditional, liver-specific ?-catenin knockdown (KD) mice and their wild-type littermates were challenged by feeding with a hepatotoxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet to induce chronic oxidative liver injury. Following the DDC diet, mice with ?-catenin-deficient hepatocytes demonstrate increased liver injury, indicating an important role of ?-catenin signaling for liver protection against oxidative stress. This finding was further confirmed in AML12 hepatocytes with ?-catenin signaling manipulation in vitro using paraquat, a known oxidative stress inducer. Immunofluorescence staining revealed an intense nuclear FoxO3 staining in ?-catenin-deficient livers, suggesting active FoxO3 signaling in response to DDC-induced liver injury when compared with wild-type controls. Consistently, FoxO3 target genes p27 and Bim were significantly induced in ?-catenin KD livers. Conversely, SGK1, a ?-catenin target gene, was significantly impaired in ?-catenin KD hepatocytes that failed to inactivate FoxO3. Furthermore, shRNA-mediated deletion of FoxO3 increased hepatocyte resistance to oxidative stress-induced apoptosis, confirming a proapoptotic role of FoxO3 in the stressed liver. Our findings suggest that Wnt/?-catenin signaling is required for hepatocyte protection against oxidative stress-induced apoptosis. The inhibition of FoxO through its phosphorylation by ?-catenin-induced SGK1 expression reduces the apoptotic function of FoxO3, resulting in increased hepatocyte survival. These findings have relevance for future therapies directed at hepatocyte protection, regeneration, and anti-cancer treatment.
  • |*Apoptosis [MESH]
  • |*Oxidative Stress [MESH]
  • |*Wnt Signaling Pathway [MESH]
  • |Animals [MESH]
  • |Apoptosis Regulatory Proteins/genetics/metabolism [MESH]
  • |Cell Line [MESH]
  • |Cell Nucleus/metabolism [MESH]
  • |Chemical and Drug Induced Liver Injury/metabolism/pathology [MESH]
  • |Forkhead Box Protein O3 [MESH]
  • |Forkhead Transcription Factors/genetics/*metabolism [MESH]
  • |Gene Expression [MESH]
  • |Gene Expression Regulation [MESH]
  • |Gene Knockdown Techniques [MESH]
  • |Hepatocytes/drug effects/*physiology [MESH]
  • |Immediate-Early Proteins/genetics/metabolism [MESH]
  • |Liver/metabolism/pathology [MESH]
  • |Mice [MESH]
  • |Mice, Transgenic [MESH]
  • |Paraquat/pharmacology [MESH]
  • |Phosphorylation [MESH]
  • |Protein Processing, Post-Translational [MESH]
  • |Protein Serine-Threonine Kinases/genetics/metabolism [MESH]
  • |Pyridines [MESH]


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