In 2015, a team of researchers found that some mutant zebrafish that lack blood cells including immune cells are unable to regenerate lost tissues. Zebrafish are particularly good at this to the extent that they can replace damaged or lost body parts with exact replicas of the originals. Our study reveals that proper levels of Il1b signaling and tissue inflammation, which are tuned by macrophages, play a crucial role in tissue regeneration.Īnimals and other multicellular organisms all have at least some ability to regenerate lost or wounded tissues.
We further show that Il1b plays an essential role in normal fin fold regeneration by regulating expression of regeneration-induced genes. 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. Here, we found that the apoptosis phenotype is induced by prolonged expression of interleukin 1 beta ( il1b). We have previously reported that myeloid-defective zebrafish mutants display apoptosis of regenerative cells during fin fold regeneration.
Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated.
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