ArticleNature medicine2010
Pharmacological correction of a defect in PPAR-gamma signaling ameliorates disease severity in Cftr-deficient mice.
Article in Nature medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 94 citations in OpenAlex.
- Fenretinide differentially modulates the levels of long- and very long-chain ceramides by downregulating Cers5 enzyme: evidence from bench to bedside.Journal of molecular medicine (Berlin, Germany) · 2017Trial
- Novel keto-phospholipids are generated by monocytes and macrophages, detected in cystic fibrosis, and activate peroxisome proliferator-activated receptor-γ.The Journal of biological chemistry · 2012Trial
- Review
- The Versatile Role of Peroxisome Proliferator-Activated Receptors in Immune-Mediated Intestinal Diseases.Cells · 2024Review
- The Use of Artificial Sputum Media to Enhance Investigation and Subsequent Treatment of Cystic Fibrosis Bacterial Infections.Microorganisms · 2022Review
- Carbonic anhydrase and soluble adenylate cyclase regulation of cystic fibrosis cellular phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- The Gut-Lung Axis in Cystic Fibrosis.Journal of bacteriology · 2021Review
- The role of essential fatty acids in cystic fibrosis and normalizing effect of fenretinide.Cellular and molecular life sciences : CMLS · 2020Review
- Review: Pathogenesis of cholestatic liver diseases.World journal of hepatology · 2020Review
- UPR modulation of host immunity by Pseudomonas aeruginosa in cystic fibrosis.Clinical science (London, England : 1979) · 2020Article
- Resveratrol restores intracellular transport in cystic fibrosis epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Targeting the Heme Oxygenase 1/Carbon Monoxide Pathway to Resolve Lung Hyper-Inflammation and Restore a Regulated Immune Response in Cystic Fibrosis.Frontiers in pharmacology · 2020Review
- Impaired Intestinal Farnesoid X Receptor Signaling in Cystic Fibrosis Mice.Cellular and molecular gastroenterology and hepatology · 2020Article
- Bromide alleviates fatty acid-induced lipid accumulation in mouse primary hepatocytes through the activation of PPARα signals.Journal of cellular and molecular medicine · 2019Article
- Article
- Enteric Microbiota⁻Gut⁻Brain Axis from the Perspective of Nuclear Receptors.International journal of molecular sciences · 2018Review
- PPARγ Modulates Long Chain Fatty Acid Processing in the Intestinal Epithelium.International journal of molecular sciences · 2017Article
- 15-hydroxyprostaglandin dehydrogenase (15-PGDH) prevents lipopolysaccharide (LPS)-induced acute liver injury.PloS one · 2017Article
- Liberating Chiral Lipid Mediators, Inflammatory Enzymes, and LIPID MAPS from Biological Grease.The Journal of biological chemistry · 2016Review
- Intestinal PPARγ signalling is required for sympathetic nervous system activation in response to caloric restriction.Scientific reports · 2016Article
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7 authors at 1 institution in 1 country.
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Abstract
Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (encoded by Cftr) that impair its role as an apical chloride channel that supports bicarbonate transport. Individuals with cystic fibrosis show retained, thickened mucus that plugs airways and obstructs luminal organs as well as numerous other abnormalities that include inflammation of affected organs, alterations in lipid metabolism and insulin resistance. Here we show that colonic epithelial cells and whole lung tissue from Cftr-deficient mice show a defect in peroxisome proliferator-activated receptor-gamma (PPAR-gamma, encoded by Pparg) function that contributes to a pathological program of gene expression. Lipidomic analysis of colonic epithelial cells suggests that this defect results in part from reduced amounts of the endogenous PPAR-gamma ligand 15-keto-prostaglandin E(2) (15-keto-PGE(2)). Treatment of Cftr-deficient mice with the synthetic PPAR-gamma ligand rosiglitazone partially normalizes the altered gene expression pattern associated with Cftr deficiency and reduces disease severity. Rosiglitazone has no effect on chloride secretion in the colon, but it increases expression of the genes encoding carbonic anhydrases 4 and 2 (Car4 and Car2), increases bicarbonate secretion and reduces mucus retention. These studies reveal a reversible defect in PPAR-gamma signaling in Cftr-deficient cells that can be pharmacologically corrected to ameliorate the severity of the cystic fibrosis phenotype in mice.
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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.