期刊
DEVELOPMENTAL CELL
卷 31, 期 1, 页码 48-60出版社
CELL PRESS
DOI: 10.1016/j.devcel.2014.08.002
关键词
-
资金
- NIH Office of Research Infrastructure Programs [P40 OD010440]
- NIH [R01 GM054657]
Reactive oxygen species (ROS) such as hydrogen peroxide are generated at wound sites and act as long-range signals in wound healing. The roles of other ROS in wound repair are little explored. Here, we reveal a cytoprotective role for mitochondrial ROS (mtROS) in Caenorhabditis elegans skin wound healing. We show that skin wounding causes local production of mtROS superoxide at the wound site. Inhibition of mtROS levels by mitochondrial superoxide-specific antioxidants blocks actin-based wound closure, whereas elevation of mtROS promotes wound closure and enhances survival of mutant animals defective in wound healing. mtROS act downstream of wound-triggered Ca2+ influx. We find that the mitochondrial calcium uniporter MCU-1 is essential for rapid mitochondria! Ca2+ uptake and mtROS production after wounding. mtROS can promote wound closure by local inhibition of Rho GTPase activity via a redox-sensitive motif. These findings delineate a pathway acting via mtROS that promotes cytoskeletal responses in wound healing.
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