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XB-ART-46493
Nat Cell Biol February 1, 2013; 15 (2): 222-8.

Amputation-induced reactive oxygen species are required for successful Xenopus tadpole tail regeneration.

Love NR , Chen Y , Ishibashi S , Kritsiligkou P , Lea R , Koh Y , Gallop JL , Dorey K , Amaya E .


Abstract
Understanding the molecular mechanisms that promote successful tissue regeneration is critical for continued advancements in regenerative medicine. Vertebrate amphibian tadpoles of the species Xenopus laevis and Xenopus tropicalis have remarkable abilities to regenerate their tails following amputation, through the coordinated activity of numerous growth factor signalling pathways, including the Wnt, Fgf, Bmp, Notch and TGF-β pathways. Little is known, however, about the events that act upstream of these signalling pathways following injury. Here, we show that Xenopus tadpole tail amputation induces a sustained production of reactive oxygen species (ROS) during tail regeneration. Lowering ROS levels, using pharmacological or genetic approaches, reduces the level of cell proliferation and impairs tail regeneration. Genetic rescue experiments restored both ROS production and the initiation of the regenerative response. Sustained increased ROS levels are required for Wnt/β-catenin signalling and the activation of one of its main downstream targets, fgf20 (ref. 7), which, in turn, is essential for proper tail regeneration. These findings demonstrate that injury-induced ROS production is an important regulator of tissue regeneration.

PubMed ID: 23314862
PMC ID: PMC3728553
Article link: Nat Cell Biol
Grant support: [+]
Genes referenced: aopep ctnnb1 cyba fgf20 hpse mcidas myc notch1 nxn rpl8 spib
Morpholinos: cyba MO1 fgf20 MO1 fgf20 MO2 spib MO1


Article Images: [+] show captions
References:
, 2003, Pubmed [+]


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