ArticleThe Journal of pharmacology and experimental therapeutics2015
Aryl hydrocarbon receptor-dependent stanniocalcin 2 induction by cinnabarinic acid provides cytoprotection against endoplasmic reticulum and oxidative stress.
Article in The Journal of pharmacology and experimental therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 49 citations in OpenAlex.
- Overexpression ofInternational journal of molecular sciences · 2026Article
- Cinnabarinic acid regulates the barrier function and inflammatory reactions in primary chicken intestinal epithelial cells with hyperthermia treatment via the aryl hydrocarbon receptor.Veterinary research communications · 2026Article
- Cell Signaling by Tryptophan Catabolism.Biochemistry · 2026Review
- The aryl hydrocarbon receptor: structure, signaling, physiology and pathology.Signal transduction and targeted therapy · 2026Review
- Production, Mechanisms, and Therapeutic Strategies of Tryptophan Metabolites in CNS Diseases.Molecular neurobiology · 2025Review
- Impact of Hericium erinaceus and Ganoderma lucidum metabolites on AhR activation in neuronal HT-22 cells.Pharmacological reports : PR · 2025Article
- Activation of the aryl hydrocarbon receptor with structurally diverse ligands suppresses class switch to immunoglobulin A.BMC research notes · 2025Article
- Multi-omics profiling of dairy cattle oxidative stress identifies hindgut-derived Phascolarctobacterium succinatutens exhibiting antioxidant activity.NPJ biofilms and microbiomes · 2025Article
- Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating aryl hydrocarbon receptor-dependent AMPK signaling.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Diverse Physiological Roles of Kynurenine Pathway Metabolites: Updated Implications for Health and Disease.Metabolites · 2025Review
- Predictive Value ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Developmental toxicity of alkylated PAHs and substituted phenanthrenes: Structural nuances drive diverse toxicity and AHR activation.Chemosphere · 2025Article
- The role of bHLH-PAS transcription factors in endoplasmic reticulum stress.Frontiers in molecular biosciences · 2025Review
- Integrative Bulk and Single-Cell Transcriptomic Profiling Reveals Oxidative Stress-Related Genes and Potential Therapeutic Targets in Osteoarthritis.Mediators of inflammation · 2025Article
- Stanniocalcin Protein Expression in Female Reproductive Organs: Literature Review and Public Cancer Database Analysis.Endocrinology · 2024Review
- Stanniocalcin 2 governs cancer cell adaptation to nutrient insufficiency through alleviation of oxidative stress.Cell death & disease · 2024Article
- Stanniocalcin 2 governs cancer cell adaptation to nutrient insufficiency through alleviation of oxidative stress.Research square · 2024Article
- Role of ERK1/2 Signaling in Cinnabarinic Acid-Driven Stanniocalcin 2-Mediated Protection against Alcohol-Induced Apoptosis.The Journal of pharmacology and experimental therapeutics · 2023Article
- Role of Hepatic Aryl Hydrocarbon Receptor in Non-Alcoholic Fatty Liver Disease.Receptors (Basel, Switzerland) · 2023Article
- Cinnabarinic Acid Provides Hepatoprotection Against Nonalcoholic Fatty Liver Disease.The Journal of pharmacology and experimental therapeutics · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The aryl hydrocarbon receptor (AhR) is a cytosolic ligand-activated transcription factor historically known for its role in xenobiotic metabolism. Although AhR activity has previously been shown to play a cytoprotective role against intrinsic apoptotic stimuli, the underlying mechanism by which AhR confers cytoprotection against apoptosis is largely unknown. Here, we demonstrate that activation of AhR by the tryptophan catabolite cinnabarinic acid (CA) directly upregulates expression of stanniocalcin 2 (Stc2) to elicit cytoprotection against apoptosis induced by endoplasmic reticulum stress and oxidative stress. Chromatin immunoprecipitation studies demonstrated that CA treatment induces direct AhR binding to a region of the Stc2 promoter containing multiple xenobiotic response elements. Using isolated primary hepatocytes from AhR wild-type (AhR floxed) and liver-specific AhR conditional knockout mice, we showed that pretreatment with CA conferred cytoprotection against hydrogen peroxide (H(2)O(2))-, thapsigargin-, and ethanol-induced apoptosis in an AhR-dependent manner. Furthermore, suppressing Stc2 expression using RNA interference confirmed that the cytoprotective properties of CA against H(2)O(2), thapsigargin, and ethanol injury were absolutely dependent on Stc2. Immunochemistry revealed the presence of Stc2 in the endoplasmic reticulum and on the cell surface, consistent with Stc2 secretion and autocrine and/or paracrine signaling. Finally, in vivo data using a mouse model of acute alcohol hepatotoxicity demonstrated that CA provided cytoprotection against ethanol-induced apoptosis, hepatic microvesicular steatosis, and liver injury. Collectively, our data uncovered a novel mechanism for AhR-mediated cytoprotection in the liver that is dependent on CA-induced Stc2 activity.
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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.