ArticlePurinergic signalling2015
Lipoapoptosis induced by saturated free fatty acids stimulates monocyte migration: a novel role for Pannexin1 in liver cells.
Article in Purinergic signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Ultrastructural Characterization of Pannexin 1 Expression Along the Rat Nephron.International journal of molecular sciences · 2026Article
- PANX1-mediated ATP release confers FAM3A's suppression effects on hepatic gluconeogenesis and lipogenesis.Military Medical Research · 2024Article
- Hepatic Macrophages as Targets for the MSC-Based Cell Therapy in Non-Alcoholic Steatohepatitis.Biomedicines · 2023Review
- Pannexin1 channels in the liver: an open enemy.Frontiers in cell and developmental biology · 2023Review
- Hepatic pannexin-1 mediates ST2Clinical and translational medicine · 2022Article
- β-hydroxybutyrate impairs monocyte functionFrontiers in veterinary science · 2022Article
- Pannexin Channel Regulation of Cell Migration: Focus on Immune Cells.Frontiers in immunology · 2021Review
- Protein Phosphatase 4 Promotes Hepatocyte Lipoapoptosis by Regulating RAC1/MLK3/JNK Pathway.Oxidative medicine and cellular longevity · 2021Article
- Review
- Possible association of arrestin domain-containing protein 3 and progression of non-alcoholic fatty liver disease.International journal of medical sciences · 2019Article
- Danger-Associated Molecular Patterns (DAMPs): Molecular Triggers for Sterile Inflammation in the Liver.International journal of molecular sciences · 2018Review
- Genetic ablation of pannexin1 counteracts liver fibrosis in a chemical, but not in a surgical mouse model.Archives of toxicology · 2018Article
- Apoptosis and non-alcoholic fatty liver diseases.World journal of gastroenterology · 2018Review
- Protective effect of genetic deletion of pannexin1 in experimental mouse models of acute and chronic liver disease.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Dual role of protein tyrosine phosphatase 1B in the progression and reversion of non-alcoholic steatohepatitis.Molecular metabolism · 2018Article
- Interactions of Pannexin1 channels with purinergic and NMDA receptor channels.Biochimica et biophysica acta. Biomembranes · 2018Review
- Pannexin1 as mediator of inflammation and cell death.Biochimica et biophysica acta. Molecular cell research · 2017Review
- The Immune Landscape in Nonalcoholic Steatohepatitis.Immune network · 2016Review
- Jiang Tang Xiao Ke Granule, a Classic Chinese Herbal Formula, Improves the Effect of Metformin on Lipid and Glucose Metabolism in Diabetic Mice.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- The effects of propolis supplementation on metabolic parameters: A systematic review and meta-analysis of randomized controlled clinical trials.Avicenna journal of phytomedicineReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Recruitment of monocytes in the liver is a key pathogenic feature of hepatic inflammation in nonalcoholic steatohepatitis (NASH), but the mechanisms involved are poorly understood. Here, we studied migration of human monocytes in response to supernatants obtained from liver cells after inducing lipoapoptosis with saturated free fatty acids (FFA). Lipoapoptotic supernatants stimulated monocyte migration with the magnitude similar to a monocyte chemoattractant protein, CCL2 (MCP-1). Inhibition of c-Jun NH2-terminal kinase (JNK) in liver cells with SP600125 blocked migration of monocytes in a dose-dependent manner, indicating that JNK stimulates release of chemoattractants in lipoapoptosis. Notably, treatment of supernatants with Apyrase to remove ATP potently inhibited migration of THP-1 monocytes and partially blocked migration of primary human monocytes. Inhibition of the CCL2 receptor (CCR2) on THP-1 monocytes with RS102895, a specific CCR2 inhibitor, did not block migration induced by lipoapoptotic supernatants. Consistent with these findings, lipoapoptosis stimulated pathophysiological extracellular ATP (eATP) release that increased supernatant eATP concentration from 5 to ~60 nM. Importantly, inhibition of Panx1 expression in liver cells with short hairpin RNA (shRNA) decreased supernatant eATP concentration and inhibited monocyte migration, indicating that monocyte migration is mediated in part by Panx1-dependent eATP release. Moreover, JNK inhibition decreased supernatant eATP concentration and inhibited Pannexin1 activation, as determined by YoPro-1 uptake in liver cells in a dose-dependent manner. These results suggest that JNK regulates activation of Panx1 channels, and provide evidence that Pannexin1-dependent pathophysiological eATP release in lipoapoptosis is capable of stimulating migration of human monocytes, and may participate in the recruitment of monocytes in chronic liver injury induced by saturated FFA.
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