Transient inflammatory response mediated by interleukin-1β is required for proper regeneration in zebrafish fin fold

被引:103
作者
Hasegawa, Tomoya [1 ]
Hall, Christopher J. [2 ]
Crosier, Philip S. [2 ]
Abe, Gembu [3 ]
Kawakami, Koichi [3 ]
Kudo, Akira [1 ]
Kawakami, Atsushi [1 ]
机构
[1] Tokyo Inst Technol, Sch Biosci & Biotechnol, Midori Ku, Tokyo, Japan
[2] Univ Auckland, Sch Med Sci, Dept Mol Med & Pathol, Auckland, New Zealand
[3] SOKENDAI, Div Mol & Dev Biol, Natl Inst Genet & Dept Genet, Mishima, Shizuoka, Japan
基金
日本学术振兴会;
关键词
TISSUE REGENERATION; SIGNAL-TRANSDUCTION; HEART REGENERATION; CELL-DEATH; INJURY; MACROPHAGES; RESOLUTION; EXPRESSION; MIGRATION; FAMILY;
D O I
10.7554/eLife.22716
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated. We have previously reported that myeloid-defective zebrafish mutants display apoptosis of regenerative cells during fin fold regeneration. Here, we found that the apoptosis phenotype is induced by prolonged expression of interleukin 1 beta (il1b). Myeloid cells are considered to be the principal source of Il1b, but we show that epithelial cells express il1b in response to tissue injury and initiate the inflammatory response, and that its resolution by macrophages is necessary for survival of regenerative cells. We further show that Il1b plays an essential role in normal fin fold regeneration by regulating expression of regeneration-induced genes. Our study reveals that proper levels of Il1b signaling and tissue inflammation, which are tuned by macrophages, play a crucial role in tissue regeneration.
引用
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页数:22
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