title: Reactive oxygen species generated from skeletal muscles are required for gecko tail regeneration.
abstract: Reactive oxygen species (ROS) participate in various physiological and pathological functions following generation from different types of cells. Here we explore ROS functions on spontaneous tail regeneration using gecko model. ROS were mainly produced in the skeletal muscle after tail amputation, showing a temporal increase as the regeneration proceeded. Inhibition of the ROS production influenced the formation of autophagy in the skeletal muscles, and as a consequence, the length of the regenerating tail. Transcriptome analysis has shown that NADPH oxidase (NOX2) and the subunits (p40(phox) and p47(phox)) are involved in the ROS production. ROS promoted the formation of autophagy through regulation of both ULK and MAPK activities. Our results suggest that ROS produced by skeletal muscles are required for the successful gecko tail regeneration.
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.|Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China.
authors: Qing
authors: Q
authors: Zhang
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Yingjie
authors: Y
authors: Wang
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Lili
authors: L
authors: Man
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Ziwen
authors: Z
authors: Zhu
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Xue
authors: X
authors: Bai
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Sumei
authors: S
authors: Wei
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Yan
authors: Y
authors: Liu
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Mei
authors: M
authors: Liu
authors: Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China.
authors: Xiaochuan
authors: X
authors: Wang
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Xiaosong
authors: X
authors: Gu
authors: Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, PR China.
authors: Yongjun
authors: Y
authors: Wang
mesh_terms: D000818:Animals; D020869:Gene Expression Profiling; D008116:Lizards / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism*; D019255:NADPH Oxidases / Q000032:analysis / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012038:Regeneration; D013623:Tail / Q000502:physiology*
chemical_list: D017382:Reactive Oxygen Species; D019255:NADPH Oxidases