ArticleMolecular medicine reports2019
17β‑Estradiol protects against interleukin‑1β‑induced apoptosis in rat nucleus pulposus cells via the mTOR/caspase‑3 pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
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- Oestrogen and Vibration Improve Intervertebral Disc Cell Viability and Decrease Catabolism in Bovine Organ Cultures.International journal of molecular sciences · 2023Article
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- Role of signal transduction pathways in IL-1β-induced apoptosis: Pathological and therapeutic aspects.Immunity, inflammation and disease · 2023Review
- Emerging role and therapeutic implication of mTOR signalling in intervertebral disc degeneration.Cell proliferation · 2023Review
- Upregulation of SIRT1 by Evodiamine activates PI3K/AKT pathway and blocks intervertebral disc degeneration.Molecular medicine reports · 2022Article
- Taurine attenuates ER stress‑associated apoptosis and catabolism in nucleus pulposus cells.Molecular medicine reports · 2022Article
- Hydroxysafflor Yellow A (HSYA) Protects Endplate Chondrocytes Against IL-1Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Correlation Analysis between Tamoxifen and Lumbar Intervertebral Disc Degeneration: A Retrospective Case-Control Study.Pain research & management · 2022Article
- Depleted Long Noncoding RNA GAS5 Relieves Intervertebral Disc Degeneration via microRNA-17-3p/Ang-2.Oxidative medicine and cellular longevity · 2022Article
- Effects of Androgen Receptor Overexpression on Chondrogenic Ability of Rabbit Articular Chondrocytes.Tissue engineering and regenerative medicine · 2021Article
- Intervertebral Disc Degeneration Induced by Needle Puncture and Ovariectomy: A Rat Coccygeal Model.BioMed research international · 2021Article
- 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
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IVDD) is the main pathological basis of spinal degenerative diseases, and aberrant apoptosis of nucleus pulposus cells (NPCs) is the main cellular process that causes IVDD. In our previous studies, 17β‑estradiol (E2) was demonstrated to protect rat NPCs from interleukin‑1β (IL‑1β)‑induced apoptosis via the PI3K/Akt signaling pathway. However, the downstream signaling pathway of PI3K/Akt is currently unclear. The present study aimed to explore the signaling pathways that are downstream of the PI3K/Akt pathway, including mTOR, NF‑κB and glycogen synthase kinase‑3β (GSK‑3β). Annexin V/propidium iodide double staining was used to determine the incidence of apoptosis. Cell Counting kit‑8 and MTS assays were used to determine the proliferation and viability of NPCs, respectively. Cellular binding was evaluated using a cell‑collagen binding assay. Western blotting was used to determine the protein expression levels of mTOR, NF‑κB and GSK‑3β, and their phosphorylation levels, as well as the expression levels of active caspase‑3. The results revealed that IL‑1β induced NPC apoptosis and increased the early apoptotic rate of NPCs. However, E2 reduced the early apoptosis of NPCs induced by IL‑1β. In addition, E2 suppressed the decrease in cell viability and binding ability caused by IL‑1β cytotoxicity. Western blotting revealed that E2 also reduced the expression of activated caspase‑3, and increased the expression of activated mTOR. As a specific inhibitor of mTOR, rapamycin effectively attenuated the effects of E2. These findings indicated that E2 protected NPCs against apoptosis via activation of the mTOR/caspase‑3 pathway.
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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.