ArticleEndocrinology and metabolism (Seoul, Korea)2023
Phospholipase C-γ as a Potential Therapeutic Target for Graves' Orbitopathy.
Article in Endocrinology and metabolism (Seoul, Korea), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Molecular subtyping of colorectal cancer based on inositol metabolism identifies PLCG2 as a key prognostic biomarker.BMC gastroenterology · 2026Article
- Selenium-enriched yeast improves gut health in broilers by modulating the gut microbiota-metabolites-intestinal mucosal immunity axis.Journal of animal science · 2026Article
- Mammalian PI-Phospholipase C Isozymes: Structural and Functional Insights and Roles in Health and Disease.Medicina (Kaunas, Lithuania) · 2025Review
- Dynamic transition of Tregs to cytotoxic phenotype amid systemic inflammation in Graves' ophthalmopathy.JCI insight · 2024Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgruoundPhospholipase C-γ (PLC-γ) plays a crucial role in immune responses and is related to the pathogenesis of various inflammatory disorders. In this study, we investigated the role of PLC-γ and the therapeutic effect of the PLC-specific inhibitor U73122 using orbital fibroblasts from patients with Graves' orbitopathy (GO).
methodsThe expression of phospholipase C gamma 1 (PLCG1) and phospholipase C gamma 2 (PLCG2) was evaluated using polymerase chain reaction in GO and normal orbital tissues/fibroblasts. The primary cultures of orbital fibroblasts were treated with non-toxic concentrations of U73122 with or without interleukin (IL)-1β to determine its therapeutic efficacy. The proinflammatory cytokine levels and activation of downstream signaling molecules were determined using Western blotting.
resultsPLCG1 and PLCG2 mRNA expression was significantly higher in GO orbital tissues than in controls (P<0.05). PLCG1 and PLCG2 mRNA expression was significantly increased (P<0.05) in IL-1β, tumor necrosis factor-α, and a cluster of differentiation 40 ligand-stimulated GO fibroblasts. U73122 significantly inhibited the IL-1β-induced expression of proinflammatory molecules, including IL-6, IL-8, monocyte chemoattractant protein-1, cyclooxygenase-2, and intercellular adhesion molecule-1 (ICAM-1), and phosphorylated protein kinase B (p-Akt) and p38 (p-p38) kinase in GO fibroblasts, whereas it inhibited IL-6, IL-8, and ICAM-1, and p-Akt and c-Jun N-terminal kinase (p-JNK) in normal fibroblasts (P<0.05).
conclusionPLC-γ-inhibiting U73122 suppressed the production of proinflammatory cytokines and the phosphorylation of Akt and p38 kinase in GO fibroblasts. This study indicates the implications of PLC-γ in GO pathogenesis and its potential as a therapeutic target for GO.
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