ArticleJournal of inflammation (London, England)2011
Parthenolide inhibits ERK and AP-1 which are dysregulated and contribute to excessive IL-8 expression and secretion in cystic fibrosis cells.
Article in Journal of inflammation (London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Parthenolide and Its Derivatives in the Treatment of Respiratory Tract Diseases: Therapeutic Effects and Molecular Mechanisms.Drug design, development and therapy · 2026Review
- The Tricky Connection between Extracellular Vesicles and Mitochondria in Inflammatory-Related Diseases.International journal of molecular sciences · 2023Review
- Anti-Inflammatory and Immunoregulatory Action of Sesquiterpene Lactones.Molecules (Basel, Switzerland) · 2022Review
- Review
- Parthenolide Has Negative Effects on In Vitro Enhanced Osteogenic Phenotypes by Inflammatory Cytokine TNF-α via Inhibiting JNK Signaling.International journal of molecular sciences · 2020Article
- Mitochondrial Stress Responses and "Mito-Inflammation" in Cystic Fibrosis.Frontiers in pharmacology · 2020Review
- Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) in Human Lung Microvascular Endothelial Cells Controls Oxidative Stress, Reactive Oxygen-Mediated Cell Signaling and Inflammatory Responses.Frontiers in physiology · 2020Article
- Article
- Molecular characterization of gene regulatory networks in primary human tracheal and bronchial epithelial cells.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2018Article
- The natural sesquiterpene lactones arglabin, grosheimin, agracin, parthenolide, and estafiatin inhibit T cell receptor (TCR) activation.Phytochemistry · 2018Article
- Mesenchymal Stem Cell Soluble Mediators and Cystic Fibrosis.Journal of stem cell research & therapy · 2017Article
- Interleukin-17 Pathophysiology and Therapeutic Intervention in Cystic Fibrosis Lung Infection and Inflammation.Infection and immunity · 2016Article
- Article
- Parthenolide Induces Apoptosis in Committed Progenitor AML Cell line U937 via Reduction in Osteopontin.Reports of biochemistry & molecular biology · 2016Article
- Parthenolide induces MITF-M downregulation and senescence in patient-derived MITF-M(high) melanoma cell populations.Oncotarget · 2016Article
- Dysregulated Chemokine Signaling in Cystic Fibrosis Lung Disease: A Potential Therapeutic Target.Current drug targets · 2016Review
- Inhibiting IκBβ-NFκB signaling attenuates the expression of select pro-inflammatory genes.Journal of cell science · 2015Article
- Anti-inflammatory and antiosteoclastogenic activities of parthenolide on human periodontal ligament cells in vitro.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- The NF-κB inhibitory proteins IκBα and IκBβ mediate disparate responses to inflammation in fetal pulmonary endothelial cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- CFTR activity and mitochondrial function.Redox biology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundExcessive secretion of IL-8 characterizes cystic fibrosis (CF). This has been attributed to excessive activation of epithelial cell I-κB Kinase and/or NFκB. Maximum IL-8 production requires 3 cooperative mechanisms: 1) release of the promoter from repression; 2) activation of transcription by NFκB and AP-1; 3) stabilization of mRNA by p38-MAPK. Little is known about regulation of IL-8 by MAPKs or AP-1 in CF.
methodsWe studied our hypothesis in vitro using 3-cellular models. Two of these models are transformed cell lines with defective versus normal cystic fibrosis transmembrane conductance regulator (CFTR) expression: an antisense/sense transfected cell line and the patient derived IB3-1/S9. In the third series of studies, we studied primary necropsy human tracheal epithelial cells treated with an inhibitor of CFTR function. All cell lines were pretreated with parthenolide and then stimulated with TNFα and/or IL-1β.
resultsIn response to stimulation with TNFα and/or IL-1β, IL-8 production and mRNA expression was greater in CF-type cells than in non-CF controls. This was associated with enhanced phosphorylation of p38, ERK1/2 and JNK and increased activation of AP-1. Since we previously showed that parthenolide inhibits excessive IL-8 production by CF cells, we evaluated its effects on MAPK and AP-1 activation and showed that parthenolide inhibited ERK and AP-1 activation. Using a luciferase promoter assay, our studies showed that parthenolide decreased activation of the IL-8 promoter in CF cells stimulated with TNFα/IL-1β.
conclusionsIn addition to NFκB MAPKs ERK, JNK and p38 and the transcription factor AP-1 are also dysregulated in CF epithelial cells. Parthenolide inhibited both NFκB and MAPK/AP-1 pathways contributing to the inhibition of IL-8 production.
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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.