ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2016
Bile acids regulate intestinal cell proliferation by modulating EGFR and FXR signaling.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 117 citations in OpenAlex.
- Dietary Acidifier Modulates the Gut Microbiota-Metabolic Axis to Improve Intestinal Health, Yolk Fatty Acid Profiles, and Egg Quality in Laying Hens.International journal of molecular sciences · 2026Article
- Gut microbiota promote early-life digestive function in songbirds.bioRxiv : the preprint server for biology · 2026Article
- Modulation of intestinal bile acids influences colonic mucosal responses.Scientific reports · 2026Article
- Role of gut microbiota metabolites in maintaining intestinal health and preventing weaning-associated diarrhea in piglets.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Review
- Sulfated bile acid produced by a human gut commensal alleviates paediatric sepsis in mice.Nature microbiology · 2026Article
- Exploring the role of metabolic disorders and gut microbiome in immune checkpoint regulation in cancer: PI3K/AKT/mTOR focus.Journal of physiology and biochemistry · 2026Review
- Gut microbiome-produced bile acid metabolite lengthens the circadian period in host intestinal cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Capecitabine combined with fecal microbiota transplantation prevents colorectal cancer progression through correction of microbial dysbiosis and immune regulation.Scientific reports · 2026Article
- Pathogenesis and intervention strategies for metabolic dysfunction-associated fatty liver disease from the perspective of the gut-microbiota-liver axis.Frontiers in immunology · 2026Review
- Moderate increase in dietary fat induces alterations of microbiota and metabolome along the digestive tract prior to systemic metabolic changes: insights from a pig model.Gut microbes · 2025Article
- Breastfeeding and infant gut microbiota: influence of bioactive components.Gut microbes · 2025Review
- Integrative transcriptomics and metabolomics reveal neuroendocrine-lipid crosstalk and adenosine signaling in broiler under heat stress.BMC genomics · 2025Article
- Common mechanisms of Gut microbe-based strategies for the treatment of intestine-related diseases: based on multi-target interactions with the intestinal barrier.Cell communication and signaling : CCS · 2025Review
- Crosstalk Between Bile Acids and Intestinal Epithelium: Multidimensional Roles of Farnesoid X Receptor and Takeda G Protein Receptor 5.International journal of molecular sciences · 2025Review
- Effects of Bile Acids on Growth Performance, Hepatopancreatic Antioxidant Capacity, Intestinal Immune-Related Gene Expression, and Gut Microbiota ofAnimals : an open access journal from MDPI · 2025Article
- Analyzing the gut liver axis: a dual role of the microbiome in the genesis, progression, and treatment of liver cell carcinoma.Frontiers in microbiology · 2025Review
- Gut dysbiosis impairs intestinal renewal and lipid absorption in Scarb2 deficiency-associated neurodegeneration.Protein & cell · 2024Article
- Impact of Varying Dietary Calcium Contents on the Gut Metabolomics of Yunnan Semi-Fine Wool Sheep (Metabolites · 2024Article
- TGR5 deficiency in excitatory neurons ameliorates Alzheimer's pathology by regulating APP processing.Science advances · 2024Article
- The Role of Gut Microbiota in the Etiopathogenesis of Multiple Chronic Diseases.Antibiotics (Basel, Switzerland) · 2024Review
14 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bile acids (BAs) are synthesized in the liver and secreted into the intestine. In the lumen, enteric bacteria metabolize BAs from conjugated, primary forms into more toxic unconjugated, secondary metabolites. Secondary BAs can be injurious to the intestine and may contribute to disease. The epidermal growth factor receptor (EGFR) and the nuclear farnesoid X receptor (FXR) are known to interact with BAs. In this study we examined the effects of BAs on intestinal epithelial cell proliferation and investigated the possible roles for EGFR and FXR in these effects. We report that taurine-conjugated cholic acid (TCA) induced proliferation, while its unconjugated secondary counterpart deoxycholic acid (DCA) inhibited proliferation. TCA stimulated phosphorylation of Src, EGFR, and ERK 1/2. Pharmacological blockade of any of these pathways or genetic ablation of EGFR abrogated TCA-stimulated proliferation. Interestingly, Src or EGFR inhibitors eliminated TCA-induced phosphorylation of both molecules, suggesting that their activation is interdependent. In contrast to TCA, DCA exposure diminished EGFR phosphorylation, and pharmacological or siRNA blockade of FXR abolished DCA-induced inhibition of proliferation. Taken together, these results suggest that TCA induces intestinal cell proliferation via Src, EGFR, and ERK activation. In contrast, DCA inhibits proliferation via an FXR-dependent mechanism that may include downstream inactivation of the EGFR/Src/ERK pathway. Since elevated secondary BA levels are the result of specific bacterial modification, this may provide a mechanism through which an altered microbiota contributes to normal or abnormal intestinal epithelial cell proliferation.
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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.