ArticleZebrafish2013
Interferon-gamma directly mediates developmental biliary defects.
Article in Zebrafish, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Biliary Atresia Animal Models: Is the Needle in a Haystack?International journal of molecular sciences · 2022Review
- Hepatocyte Nuclear Factor-1Journal of the American Society of Nephrology : JASN · 2017Article
- Making It New Again: Insight Into Liver Development, Regeneration, and Disease From Zebrafish Research.Current topics in developmental biology · 2017Review
- Methylation Microarray Studies Highlight PDGFA Expression as a Factor in Biliary Atresia.PloS one · 2016Article
- Zebrafish: an important tool for liver disease research.Gastroenterology · 2015Review
- The lure of zebrafish in liver research: regulation of hepatic growth in development and regeneration.Current opinion in genetics & development · 2015Review
- Evidence from human and zebrafish that GPC1 is a biliary atresia susceptibility gene.Gastroenterology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Biliary atresia (BA) is the most common identifiable hepatobiliary disease affecting infants, in which there are defects in intra- and extrahepatic bile ducts and progressive fibrosis. Activation of interferon-gamma (IFNγ) appears to be critical in both patients with BA and in rodent models of BA. We have recently reported a zebrafish model of biliary disease that shares features with BA, in which inhibition of DNA methylation leads to intrahepatic biliary defects and activation of IFNγ target genes. Here we report that ifng genes are hypomethylated and upregulated in zebrafish larvae treated with azacytidine (azaC), an inhibitor of DNA methylation. Injection of IFNγ protein into developing zebrafish larvae leads to biliary defects, suggesting that activation of the IFNγ pathway is sufficient to cause developmental biliary defects. These defects are associated with decreased cholangiocyte proliferation and with a decrease in the expression of vhnf1 (hnf1b, tcf2), which encodes a homeodomain protein with previously reported roles in biliary development in multiple models. These results support an importance of IFNγ in mediating biliary defects, and also demonstrate the feasibility of direct injection of intact protein into developing zebrafish larvae.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.