ArticleCell cycle (Georgetown, Tex.)2015
Activation of autophagy via Ca(2+)-dependent AMPK/mTOR pathway in rat notochordal cells is a cellular adaptation under hyperosmotic stress.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Article
- Stress-response exhaustion in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2026Review
- LIPUS Promotes Calcium Oscillation and Enhances Calcium Dependent Autophagy of Chondrocytes to Alleviate Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Delta opioid peptide [D-ala2, D-leu5]-Enkephalin's ability to enhance mitophagy via TRPV4 to relieve ischemia/reperfusion injury in brain microvascular endothelial cells.Stroke and vascular neurology · 2025Article
- Overexpression of TRPV1 activates autophagy in human lens epithelial cells under hyperosmotic stress through CaInternational journal of ophthalmology · 2024Article
- Autophagy is involved in degradation of AQP1 in response to an acute decrement in tonicity.iScience · 2023Article
- Intervertebral disc cell fate during aging and degeneration: apoptosis, senescence, and autophagy.North American Spine Society journal · 2023Article
- Article
- Specific PFKFB3 Inhibitor Memorably Ameliorates Intervertebral Disc Degeneration via Inhibiting NF-Oxidative medicine and cellular longevity · 2022Article
- He-Wei Granule enhances anti-tumor activity of cyclophosphamide by changing tumor microenvironment.Chinese herbal medicines · 2022Article
- Mitochondrial quality control in intervertebral disc degeneration.Experimental & molecular medicine · 2021Review
- Role of autophagy in intervertebral disc and cartilage function: implications in health and disease.Matrix biology : journal of the International Society for Matrix Biology · 2021Review
- Comprehensive analysis of lumbar disc degeneration and autophagy-related candidate genes, pathways, and targeting drugs.Journal of orthopaedic surgery and research · 2021Article
- Kinetics of osmotic stress regulate a cell fate switch of cell survival.Science advances · 2021Article
- Review
- FV-429 induces autophagy blockage and lysosome-dependent cell death of T-cell malignancies via lysosomal dysregulation.Cell death & disease · 2021Article
- Apigenin Alleviates Intervertebral Disc DegenerationFrontiers in cell and developmental biology · 2021Article
- AMPK as a Potential Therapeutic Target for Intervertebral Disc Degeneration.Frontiers in molecular biosciences · 2021Review
- Increased Expression of Integrin Alpha 6 in Nucleus Pulposus Cells in Response to High Oxygen Tension Protects against Intervertebral Disc Degeneration.Oxidative medicine and cellular longevity · 2021Article
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7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleus pulposus (NP) cells experience hyperosmotic stress in spinal discs; however, how these cells can survive in the hostile microenvironment remains unclear. Autophagy has been suggested to maintain cellular homeostasis under different stresses by degrading the cytoplasmic proteins and organelles. Here, we explored whether autophagy is a cellular adaptation in rat notochordal cells under hyperosmotic stress. Hyperosmotic stress was found to activate autophagy in a dose- and time-dependent manner. SQSTM1/P62 expression was decreased as the autophagy level increased. Transient Ca(2+) influx from intracellular stores and extracellular space was stimulated by hyperosmotic stress. Activation of AMPK and inhibition of p70S6K were observed under hyperosmotic conditions. However, intercellular Ca(2+) chelation inhibited the increase of LC3-II and partly reversed the decrease of p70S6K. Hyperosmotic stress decreased cell viability and promoted apoptosis. Inhibition of autophagy led to SQSTM1/P62 accumulation, reduced cell viability, and accelerated apoptosis in notochordal cells under this condition. These evidences suggest that autophagy induction via the Ca(2+)-dependent AMPK/mTOR pathway might occur as an adaptation mechanism for notochordal cells under hyperosmotic stress. Thus, activating autophagy might be a promising approach to improve viability of notochordal cells in intervertebral discs.
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