TY - JOUR
T1 - Transient inflammatory response mediated by interleukin-1β is required for proper regeneration in zebrafish fin fold
AU - Hasegawa, Tomoya
AU - Hall, Christopher J.
AU - Crosier, Philip S.
AU - Abe, Gembu
AU - Kawakami, Koichi
AU - Kudo, Akira
AU - Kawakami, Atsushi
N1 - Funding Information:
We thank members of the Kawakami lab. This work was supported by grants from the Koyanagi Foundation and a Grant-in-Aid for Scientific Research (C) to A Kawakami, by the Marsden Fund grant from the Royal Society of New Zealand to C. J Hall, and by the NIG-JOINT grant from the National Institute of Genetics to A Kawakami and K Kawakami, and by the National BioResource Project from Japan Agency for Medical Research and Development (AMED) to K Kawakami. TH was supported by a fellowship from the Education Academy of Computational Life Science (ACLS) at Tokyo Institute of Technology. Japan Society for the Promotion of Science Grant-in-Aid for Scientific Research (C) Atsushi Kawakami. Japan Agency for Medical Research and Development National BioResource Project Koichi Kawakami. Royal Society of New Zealand Marsden Fund Christopher J Hall. The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
PY - 2017/2/23
Y1 - 2017/2/23
N2 - Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated. We have previously reported that myeloiddefective 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.
AB - Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated. We have previously reported that myeloiddefective 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.
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U2 - 10.7554/eLife.22716
DO - 10.7554/eLife.22716
M3 - Article
C2 - 28229859
AN - SCOPUS:85015890424
VL - 6
JO - eLife
JF - eLife
SN - 2050-084X
M1 - e22716
ER -