title: Transient inflammatory response mediated by interleukin-1β is required for proper regeneration in zebrafish fin fold.
abstract: 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 ofinterleukin 1 beta(il1b). Myeloid cells are considered to be the principal source of Il1b, but we show that epithelial cells expressil1bin 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.
authors.affiliation: School of Bioscience and Biotechnology, Tokyo Institute of Technology, Midori-ku, Japan.
authors.forename: Tomoya
authors.initials: T
authors.lastname: Hasegawa
authors.affiliation: Department of Molecular Medicine and Pathology, School of Medical Sciences, University of Auckland, Auckland, New Zealand.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Hall
authors.affiliation: Department of Molecular Medicine and Pathology, School of Medical Sciences, University of Auckland, Auckland, New Zealand.
authors.forename: Philip S
authors.initials: PS
authors.lastname: Crosier
authors.affiliation: Division of Molecular and Developmental Biology, National Institute of Genetics, and Department of Genetics, SOKENDAI (The Graduate University for Advanced Studies), Mishima, Japan.
authors.forename: Gembu
authors.initials: G
authors.lastname: Abe
authors.affiliation: Division of Molecular and Developmental Biology, National Institute of Genetics, and Department of Genetics, SOKENDAI (The Graduate University for Advanced Studies), Mishima, Japan.
authors.forename: Koichi
authors.identifier: http://orcid.org/0000-0001-9993-1435
authors.initials: K
authors.lastname: Kawakami
authors.affiliation: School of Bioscience and Biotechnology, Tokyo Institute of Technology, Midori-ku, Japan.
authors.forename: Akira
authors.initials: A
authors.lastname: Kudo
authors.affiliation: School of Bioscience and Biotechnology, Tokyo Institute of Technology, Midori-ku, Japan.
authors.forename: Atsushi
authors.identifier: http://orcid.org/0000-0001-9461-6372
authors.initials: A
authors.lastname: Kawakami
mesh_terms: D058500:Animal Fins / Q000293:injuries* / Q000502:physiology*; D000818:Animals; D007249:Inflammation; D053583:Interleukin-1beta / Q000378:metabolism*; D012038:Regeneration; D015027:Zebrafish
chemical_list: D053583:Interleukin-1beta
keywords: Interleukin 1 beta; apoptosis; developmental biology; fin fold; inflammation; macrophage; regeneration; stem cells; zebrafish