ArticleMedical science monitor : international medical journal of experimental and clinical research2016
17β-Estradiol Inhibites Tumor Necrosis Factor-α Induced Apoptosis of Human Nucleus Pulposus Cells via the PI3K/Akt Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
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- Asymmetric distribution of Modic changes in patients with lumbar disc herniation.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2023Article
- Molecular Basic of Pharmacotherapy of Cytokine Imbalance as a Component of Intervertebral Disc Degeneration Treatment.International journal of molecular sciences · 2023Review
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- Oxidative Stress Aggravates Apoptosis of Nucleus Pulposus Cells through mOxidative medicine and cellular longevity · 2022Article
- Irisin Ameliorates Intervertebral Disc Degeneration by Activating LATS/YAP/CTGF Signaling.Oxidative medicine and cellular longevity · 2022Article
- Erratum: 17β-Estradiol Inhibites Tumor Necrosis Factor-α Induced Apoptosis of Human Nucleus Pulposus Cells via the PI3K/Akt Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Liraglutide Protects Nucleus Pulposus Cells Against High-Glucose Induced Apoptosis by Activating PI3K/Akt/ mTOR/Caspase-3 and PI3K/Akt/GSK3β/Caspase-3 Signaling Pathways.Frontiers in medicine · 2021Article
- Influence of Gestational Hormones on the Bacteria-Induced Cytokine Response in Periodontitis.Mediators of inflammation · 2021Review
- [Endoplasmic reticulum stress enhances tumor necrosis factor-Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- The protective effects of PI3K/Akt pathway on human nucleus pulposus mesenchymal stem cells against hypoxia and nutrition deficiency.Journal of orthopaedic surgery and research · 2020Article
- Kupffer Cell-Derived TNF-BioMed research international · 2020Article
- 17β‑Estradiol protects against interleukin‑1β‑induced apoptosis in rat nucleus pulposus cells via the mTOR/caspase‑3 pathway.Molecular medicine reports · 2019Article
- Resveratrol inhibits IL-1β-mediated nucleus pulposus cell apoptosis through regulating the PI3K/Akt pathway.Bioscience reports · 2019Article
- Osteogenic protein-1 attenuates nucleus pulposus cell apoptosis through activating the PI3K/Akt/mTOR pathway in a hyperosmotic culture.Bioscience reports · 2018Article
- Long non-coding RNA phosphatase and tensin homolog pseudogene 1 suppresses osteosarcoma cell growth via the phosphoinositide 3-kinase/protein kinase B signaling pathway.Experimental and therapeutic medicine · 2018Article
- Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway.Bioscience reports · 2018Article
- Protective role of 17β-estradiol on tumor necrosis factor-α-induced apoptosis in human nucleus pulposus cells.Molecular medicine reports · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Tumor necrosis factor-α (TNF-α) has been widely known to induce degeneration of nucleus pulposus cells (NPCs). 17β-estradiol (17β-E2) has been broadly proven for its function of suppressing cell apoptosis. The aim of this study is to explore whether 17β-E2 protects apoptosis of human NPCs induced by TNF-α via the PI3K/AKT pathway. MATERIAL AND METHODS NPCs were divided into four groups: control, TNF-α (100 ng/mL), TNF-α (100 ng/mL) with pretreated 17β-E2 (10 um/L), TNF-α (100 ng/mL) with pretreated 17β-E2 (10 um/L) and MK2206 (10 um/L, inhibitor of the PI3K/AKT pathway). Flow cytometry was used to measure the apoptotic incidence. Inverted phase-contrast microscopy was used to accomplish the morphological observation for apoptosis of treated cells. Additionally, Cell Counting Kit 8 (CCK-8) assay was used to detected cell proliferation. Western blot and quantitative real-time PCR (qRT-PCR) were applied to explore the expression of pro-caspase-3, caspase-3/p17, cleaved PARP, PARP, Akt, and phospho-Akt (p-Akt). RESULTS First, inverted phase-contrast microscopy, CCK-8, and flow cytometry showed that TNF-α induced marked apoptosis, which was abolished by 17β-E2. Furthermore, Western blot and qRT-PCR showed that 17β-E2 protects TNF-α which can induced apoptosis by upregulating p-Akt, whereas Akt was essentially constant. Our data revealed that p-Akt expression peaked at 24 hours in a time-dependent manner (0-48 hours) after treating with TNF-α; and the p-Akt expression generally increased in a time-dependent manner (0-48 hours) after treating with TNF-α and 17β-E2. CONCLUSIONS 17β-E2 is shown to protect NPCs against TNF-α induced apoptosis by upregulating p-Akt in the PI3K/AKT pathway. 17β-E2 generally increases expression of p-Akt.
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