ArticleProceedings of the National Academy of Sciences of the United States of America2021
Mucosal acidosis elicits a unique molecular signature in epithelia and intestinal tissue mediated by GPR31-induced CREB phosphorylation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Engineering microbial consortia for distributed signal processing.Nature communications · 2026Article
- Metabolic host-microbe crosstalk in stabilization of epithelial HIF.Microbiome · 2026Article
- Impact of Neutrophils on the Tissue Microenvironment During Intestinal Inflammation.Journal of inflammation research · 2026Review
- Spatial transcriptomics delineates potential differences in intestinal phenotypes of cardiac and classical necrotizing enterocolitis.iScience · 2025Article
- Genetically engineered bacteria as inflammatory bowel disease therapeutics.Engineering microbiology · 2024Review
- The pyruvate-GPR31 axis promotes transepithelial dendrite formation in human intestinal dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Gut Dysbiosis Drives Inflammatory Bowel Disease Through the CCL4L2-VSIR Axis in Glycogen Storage Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Chlorination of epithelial tight junction proteins by neutrophil myeloperoxidase promotes barrier dysfunction and mucosal inflammation.JCI insight · 2024Article
- Data-driven learning of structure augments quantitative prediction of biological responses.PLoS computational biology · 2024Article
- Crosstalk with renal proximal tubule cells drives acidosis-induced inflammatory response and dedifferentiation of fibroblasts via p38-singaling.Cell communication and signaling : CCS · 2024Article
- Review
- Hydrogel-encapsulation to enhance bacterial diagnosis of colon inflammation.Biomaterials · 2023Article
- Engineered calprotectin-sensing probiotics for IBD surveillance in humans.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The TNFThe American journal of pathology · 2023Article
- The hypoxic tissue microenvironment as a driver of mucosal inflammatory resolution.Frontiers in immunology · 2023Review
- Essential role for epithelial HIF-mediated xenophagy in control of Salmonella infection and dissemination.Cell reports · 2022Article
- The Hypoxia-Adenosine Link during Myocardial Ischemia-Reperfusion Injury.Biomedicines · 2022Review
- Bacterial two-component systems as sensors for synthetic biology applications.Current opinion in systems biology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Metabolic changes associated with tissue inflammation result in significant extracellular acidosis (EA). Within mucosal tissues, intestinal epithelial cells (IEC) have evolved adaptive strategies to cope with EA through the up-regulation of SLC26A3 to promote pH homeostasis. We hypothesized that EA significantly alters IEC gene expression as an adaptive mechanism to counteract inflammation. Using an unbiased RNA sequencing approach, we defined the impact of EA on IEC gene expression to define molecular mechanisms by which IEC respond to EA. This approach identified a unique gene signature enriched in cyclic AMP response element-binding protein (CREB)-regulated gene targets. Utilizing loss- and gain-of-function approaches in cultured epithelia and murine colonoids, we demonstrate that EA elicits prominent CREB phosphorylation through cyclic AMP-independent mechanisms that requires elements of the mitogen-activated protein kinase signaling pathway. Further analysis revealed that EA signals through the G protein-coupled receptor GPR31 to promote induction of FosB, NR4A1, and DUSP1. These studies were extended to an in vivo murine model in conjunction with colonization of a pH reporter
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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 Socratic graph.