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Record W2792528042 · doi:10.1093/jcag/gwy009.065

A65 HNF4A IS A KEY REGULATOR OF THE EPITHELIAL STEM CELL NICHE.

2018· article· en· W2792528042 on OpenAlexaff
Christine M. Jones, François Boudreau

Bibliographic record

VenueJournal of the Canadian Association of Gastroenterology · 2018
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicDigestive system and related health
Canadian institutionsUniversité de Sherbrooke
Fundersnot available
KeywordsVillinBiologyCell biologyPaneth cellWnt signaling pathwayStem cellCryptIntestinal epitheliumTranscriptomeGeneticsGene expressionGeneEpitheliumSmall intestineEndocrinologySignal transduction

Abstract

fetched live from OpenAlex

HNF4α is a transcriptional factor downregulated in intestinal bowel diseases (IBD). Epithelial deletion of HNF4α in the mouse intestine leads to spontaneous intestinal inflammation. Those observations suggest that HNF4α could play an important role in epithelial homeostasis. The intestinal crypt is the functional compartment responsible for the maintenance of this homeostasis. Proliferation of stem cells is essential for the mucosa healing following injuries, while Paneth cells are important regulators of this process through the secretion of stem cell niche factors including WNT3, a key activator of the canonical WNT/β-catenin pathway. We aimed to investigate if HNF4α could play an intrinsic role in stem and Paneth cells for the maintenance of the epithelial niche in intestinal crypts. Villin-Cre/HNF4αloxp/loxp and the hydroxytamoxifen (4OHT) inducible Villin-Cre ERT2/HNF4αloxp/loxp mouse models were used in this study. Isolated crypts were processed for protein and RNA isolation. Enteroids were derived from these models and used for RNAseq and qPCR experiments. Enteroids were derived from jejunal crypts of inducible Villin-Cre ERT2/HNF4αloxp/loxp mice. Induction of HNF4α deletion with 4OHT led to degeneration of these enteroids starting 5 days after the deletion, an observation reminiscent of enteroids derived from the Villin-Cre/HNF4αloxp/loxp mouse model. EdU incorporation assays showed a decrease in the proliferative rate of enteroids 4 days following HNF4α deletion. RNAseq was next performed on RNA isolated from enteroids induced for HNF4α deletion after 2 and 4 days in culture. Transcriptomic analysis identified more than a thousand of genes differentially expressed following the deletion of HNF4α under these conditions. A significant reduction of WNT3 was predicted, an observation that was further confirmed by qPCR and Western in jejunal crypts of HNF4α mutant mice. To measure the functional relevance of WNT3 reduction during enteroids degeneration, a rescue experiment was performed. WNT3A supplementation was able to maintain HNF4α deleted enteroids in culture. Transcriptomic analysis of WNT3A-treated enteroids showed rescue for 85% of the genes identified to be modulated in enteroids deleted for HNF4α. To further verify if HNF4α may contribute to Paneth cell differentiation, enteroids committed to differentiate into the Paneth lineage were deleted for HNF4α. Gene transcript expression of Paneth cell markers (Defa3, Defa5, Defa20, Defa21-22, Lyz and WNT3) were all downregulated in the absence of HNF4α as opposed to EpHB3, which was not significantly modulated. This study identifies HNF4α as a key regulator of Paneth cell function for maintenance of the epithelial stem cell niche. These observations provide a novel mechanistic loop for which the intestinal epithelial healing process could be dependent following stress-related injuries. CIHRCCC-Vertex

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.079
Threshold uncertainty score0.964

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.005
GPT teacher head0.208
Teacher spread0.203 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

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Citations0
Published2018
Admission routes1
Has abstractyes

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