ArticleInternational journal of molecular medicine2014
PE‑induced apoptosis in SMMC‑7721 cells: involvement of Erk and Stat signalling pathways.
Article in International journal of molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Phosphatidylethanolamines Are Associated with Nonalcoholic Fatty Liver Disease (NAFLD) in Obese Adults and Induce Liver Cell Metabolic Perturbations and Hepatic Stellate Cell Activation.International journal of molecular sciences · 2023Article
- Plasma lipidomics of primary biliary cholangitis and its comparison with Sjögren's syndrome.Frontiers in immunology · 2023Article
- Lipidomics combined with transcriptomic and mass spectrometry imaging analysis of the Asiatic toad (Bufo gargarizans) during metamorphosis and bufadienolide accumulation.Chinese medicine · 2022Article
- Geniposide Ameliorates Liver Fibrosis Through Reducing Oxidative Stress and Inflammatory Respose, Inhibiting Apoptosis and Modulating Overall Metabolism.Frontiers in pharmacology · 2021Article
- MicroRNA-30-3p Suppresses Inflammatory Factor-Induced Endothelial Cell Injury by Targeting TCF21.Mediators of inflammation · 2019Article
- Phosphatidylethanolamine Induces an Antifibrotic Phenotype in Normal Human Lung Fibroblasts and Ameliorates Bleomycin-Induced Lung Fibrosis in Mice.International journal of molecular sciences · 2018Article
- Phospholipids in mitochondrial dysfunction during hemorrhagic shock.Journal of bioenergetics and biomembranes · 2017Review
- Insufficient radiofrequency ablation promotes human hepatoma SMMC7721 cell proliferation by stimulating vascular endothelial growth factor overexpression.Oncology letters · 2015Article
- Tyrosol prevents ischemia/reperfusion-induced cardiac injury in H9c2 cells: involvement of ROS, Hsp70, JNK and ERK, and apoptosis.Molecules (Basel, Switzerland) · 2015Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence indicates that the redistribution of phosphatidylethanolamine (PE) across the bilayer of the plasma membrane is an important molecular marker for apoptosis. However, the effect of PE on apoptosis and the underlying mechanism of PE remain unclear. In the current study, MTT and flow cytometric assays were used to examine the effects of PE on apoptosis in SMMC‑7721 cells. The level of mitochondrial membrane potential (ΔΨm) and the expression of Bax, Bcl‑2, caspase‑3, phospho‑Erk and phospho‑Stat1/2 in SMMC‑7721 cells that were exposed to PE were also investigated. The results showed that PE inhibited proliferation, caused G0/G1 phase cell cycle arrest and induced apoptosis in SMMC‑7721 cells in a dose‑dependent manner. Rhodamine 123 staining showed that the treatment of SMMC‑7721 cells with different concentrations of PE for 24 h significantly decreased the level of ΔΨm and exerted dose‑dependent effects. Using immunofluorescence and western blotting, we found that the expression of Bax was upregulated, whereas that of Bcl‑2 was downregulated in PE‑induced apoptotic cells. In addition, these events were accompanied by an increase in caspase‑3 expression in a dose‑dependent manner following PE treatment. PE‑induced apoptosis was accompanied by a decrease in Erk phospho-rylation and by the activation of Stat1/2 phosphorylation in SMMC‑7721 cells. In conclusion, the results suggested that PE‑induced apoptosis is involved in upregulating the Bax/Bcl‑2 protein ratio and decreasing the ΔΨm. Moreover, the results showed that the Erk and Stat1/2 signalling pathways may be involved in the process of PE‑induced apoptosis.
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