ArticleCell death and differentiation2020
Prolyl hydroxylase 3 controls the intestine goblet cell generation through stabilizing ATOH1.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Integrated multi-omics reveals Enterococcus faecalis JM263 alleviates high-concentrate diet-induced hepatic injury via the gut-liver axis in goats.Microbiome · 2026Article
- Ubiquitin-Modifying Enzymes as Cell-Fate Regulators in Intestinal Inflammation.International journal of biological sciences · 2026Review
- Intestinal mucosal barrier repair and immune regulation with an AI-developed gut-restricted PHD inhibitor.Nature biotechnology · 2025Article
- Probiotic Administration Contributes to the Improvement in Intestinal Dysregulation Induced by Allergic Contact Dermatitis.Microorganisms · 2025Article
- Novel ubiquitination-related biomarkers for Crohn's disease identified by multi-omics study and experimental validation.Frontiers in immunology · 2025Article
- PHD1-3 oxygen sensors in vivo-lessons learned from gene deletions.Pflugers Archiv : European journal of physiology · 2024Review
- Effects of Hibernation on Colonic Epithelial Tissue and Gut Microbiota in Wild Chipmunks (Animals : an open access journal from MDPI · 2024Article
- Hypoxia inducible factor prolyl hydroxylases in inflammatory bowel disease.Frontiers in pharmacology · 2023Review
- Enteroendocrine System and Gut Barrier in Metabolic Disorders.International journal of molecular sciences · 2022Review
- Role of Goblet Cells in Intestinal Barrier and Mucosal Immunity.Journal of inflammation research · 2021Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal epithelia self-renew constantly and generate differentiated cells such as secretary goblet cells. The intestine goblet cells secrete gel-forming mucins that form mucus to create a barrier of defense. We reported previously that loss of prolyl hydroxylase (PHD) 3 led to disruption of the intestinal epithelial barrier function. However, the underlying mechanism remains elusive. Here, we demonstrate that PHD3 controls the generation of intestine goblet cell. We found that genetic ablation of Phd3 in mice intestine epithelial cells reduced the amount of goblet cells. Mechanistically, PHD3 bounds the E3 ubiquitin ligase HUWE1 and prevented HUWE1 from mediating ubiquitination and degradation of ATOH1, an essential driver for goblet cell differentiation. The prolyl hydroxylase activity-deficient variant PHD3(H196A) also prevented ATOH1 destruction. A genetic intestine epithelial PHD3(H196A)-knockin had no effect on ATOH1 expression or goblet cell amount in mice, suggesting that the PHD3 prolyl hydroxylase activity is dispensable for its ability to control ATOH1 expression and goblet cell generation. In dextran sulfate sodium (DSS)-induced experimental colitis, PHD3-knockout rather than PHD3(H196A)-knockin sensitized the mice to DSS treatment. Our results reveal an additional critical mechanism underlying the regulation of ATOH1 expression and goblet cell generation and highlight that PHD3 plays a role in controlling intestine goblet cell generation in a hydroxylase-independent manner.
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