2017
DOI: 10.7554/elife.22716
|View full text |Cite
|
Sign up to set email alerts
|

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 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 ti… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

11
117
1

Year Published

2017
2017
2024
2024

Publication Types

Select...
3
3
2

Relationship

0
8

Authors

Journals

citations
Cited by 125 publications
(129 citation statements)
references
References 65 publications
11
117
1
Order By: Relevance
“…We confirmed that the il-1β:GFP expression of our line was faithful to il-1β transcription by following its expression in a well-characterised tailfin transection model of inflammation and comparison to in situ hybridisation data (Ogryzko et al , 2014a; Renshaw & Loynes, 2006). Furthermore, the expression pattern of our BAC transgenic line closely matches another recently published BAC promoter driven il-1β transgenic (Hasegawa et al , 2017). The il-1β:GFP line also displayed some GFP signal in muscle and epithelial cells in the tail.…”
Section: Discussionsupporting
confidence: 83%
See 1 more Smart Citation
“…We confirmed that the il-1β:GFP expression of our line was faithful to il-1β transcription by following its expression in a well-characterised tailfin transection model of inflammation and comparison to in situ hybridisation data (Ogryzko et al , 2014a; Renshaw & Loynes, 2006). Furthermore, the expression pattern of our BAC transgenic line closely matches another recently published BAC promoter driven il-1β transgenic (Hasegawa et al , 2017). The il-1β:GFP line also displayed some GFP signal in muscle and epithelial cells in the tail.…”
Section: Discussionsupporting
confidence: 83%
“…Similar GFP expression can be seen when driven by NF-kB response elements (Kanther et al , 2011) but not by WISH, suggesting this might be off-target expression resulting from the promoter region missing some negative regulatory elements, however, it could also be specific expression that is at too low a level to be detectable by in situ hybridisation. Although previous studies have shown il-1β:GFP to be upregulated in leukocytes at a tailfin transection (Hasegawa et al , 2017), we combined the il-1β:GFP line with leukocyte specific transgenics to show that neutrophils are the first to respond at the wound, with macrophages both migrating to and upregulating il-1β:GFP at later timepoints.…”
Section: Discussionmentioning
confidence: 99%
“…Macrophages control inflammation, as their absence in irf8 mutants leads to abnormally high expression levels of pro-inflammatory cytokines il-1β and tnf-α. This is 1 similar to observations in fin regeneration 33 . In the absence of macrophages, positive feedback regulation of il-1β takes place, as indicated by more il-1β positive neutrophils and keratinocytes in the irf8 mutants and reduced il-1β mRNA levels when Il-1β function was inhibited.…”
Section: Neutrophils Are a Major Source Of Il-1β And Inhibit Regenerasupporting
confidence: 88%
“…Interestingly, in fin regeneration, lack of macrophages also leads to increased cell death. As this leads to death of tissue progenitor cells, fin regeneration is inhibited 33 .…”
Section: Neutrophils Are a Major Source Of Il-1β And Inhibit Regeneramentioning
confidence: 99%
“…To complement this genetic approach we also suppressed inflammation in wild type fish by treatment with hydrocortisone (from 7 days to 28 days post suture implantation - Figure 6A), similar to treatment regimes used in previous zebrafish studies (Hasegawa et al, 2017;Richardson et al, 2013). This inflammation dampening treatment resulted in a similar rescue of FBR and restoration of tissue repair and biomaterial integration to that seen in the csf1ra mutant scenario ( Figure 6B-F).…”
Section: Dampening the Inflammatory Response Results In Reduced Fibromentioning
confidence: 90%