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Autophagy is activated in compression-induced cell degeneration and is mediated by reactive oxygen species in nucleus pulposus cells exposed to compression.
Osteoarthritis Cartilage. 2013 Dec; 21(12):2030-8.OC

Abstract

OBJECTIVE

To determine whether autophagy contributes to the pathogenesis of degenerative disc disease (DDD) or retards the intervertebral disc (IVD) degeneration, and investigate the possible relationship between compression-induced autophagy and intracellular reactive oxygen species (ROS) in nucleus pulposus (NP) cells in vitro.

METHODS

The autophagosome and autophagy-related markers were used to explore the role of autophagy in rat NP cells under compressive stress, which were measured directly by electronic microscopy, monodansylcadaverine (MDC) staining, immunofluorescence, western blot, and indirectly by analyzing the impact of pharmacological inhibitors of autophagy such as 3-methyladenine (3-MA) and chloroquine (CQ). And the relationship between autophagy and apoptosis was investigated by Annexin-V/propidium iodide (PI)-fluorescein staining. In addition, ROS were measured to determine whether these factors are responsible for the development of compression-induced autophagy.

RESULTS

Our results indicated that rat NP cells activated autophagy in response to the same strong apoptotic stimuli that triggered apoptosis by compression. Autophagy and apoptosis were interconnected and coordinated in rat NP cells exposed to compression stimuli. Compression-induced autophagy was closely related to intracellular ROS production.

CONCLUSIONS

Enhanced degradation of damaged components of NP cells by autophagy may be a crucial survival response against mechanical overload, and extensive autophagy may trigger autophagic cell death. Regulating autophagy and reducing the generation of intracellular ROS may retard IVD degeneration.

Authors+Show Affiliations

Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24120490

Citation

Ma, K-G, et al. "Autophagy Is Activated in Compression-induced Cell Degeneration and Is Mediated By Reactive Oxygen Species in Nucleus Pulposus Cells Exposed to Compression." Osteoarthritis and Cartilage, vol. 21, no. 12, 2013, pp. 2030-8.
Ma KG, Shao ZW, Yang SH, et al. Autophagy is activated in compression-induced cell degeneration and is mediated by reactive oxygen species in nucleus pulposus cells exposed to compression. Osteoarthr Cartil. 2013;21(12):2030-8.
Ma, K. G., Shao, Z. W., Yang, S. H., Wang, J., Wang, B. C., Xiong, L. M., Wu, Q., & Chen, S. F. (2013). Autophagy is activated in compression-induced cell degeneration and is mediated by reactive oxygen species in nucleus pulposus cells exposed to compression. Osteoarthritis and Cartilage, 21(12), 2030-8. https://doi.org/10.1016/j.joca.2013.10.002
Ma KG, et al. Autophagy Is Activated in Compression-induced Cell Degeneration and Is Mediated By Reactive Oxygen Species in Nucleus Pulposus Cells Exposed to Compression. Osteoarthr Cartil. 2013;21(12):2030-8. PubMed PMID: 24120490.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Autophagy is activated in compression-induced cell degeneration and is mediated by reactive oxygen species in nucleus pulposus cells exposed to compression. AU - Ma,K-G, AU - Shao,Z-W, AU - Yang,S-H, AU - Wang,J, AU - Wang,B-C, AU - Xiong,L-M, AU - Wu,Q, AU - Chen,S-F, Y1 - 2013/10/10/ PY - 2013/02/20/received PY - 2013/09/29/revised PY - 2013/10/01/accepted PY - 2013/10/15/entrez PY - 2013/10/15/pubmed PY - 2014/7/31/medline KW - Apoptosis KW - Autophagy KW - Compression KW - Intervertebral disc KW - Nucleus pulposus cells KW - Reactive oxygen species SP - 2030 EP - 8 JF - Osteoarthritis and cartilage JO - Osteoarthr. Cartil. VL - 21 IS - 12 N2 - OBJECTIVE: To determine whether autophagy contributes to the pathogenesis of degenerative disc disease (DDD) or retards the intervertebral disc (IVD) degeneration, and investigate the possible relationship between compression-induced autophagy and intracellular reactive oxygen species (ROS) in nucleus pulposus (NP) cells in vitro. METHODS: The autophagosome and autophagy-related markers were used to explore the role of autophagy in rat NP cells under compressive stress, which were measured directly by electronic microscopy, monodansylcadaverine (MDC) staining, immunofluorescence, western blot, and indirectly by analyzing the impact of pharmacological inhibitors of autophagy such as 3-methyladenine (3-MA) and chloroquine (CQ). And the relationship between autophagy and apoptosis was investigated by Annexin-V/propidium iodide (PI)-fluorescein staining. In addition, ROS were measured to determine whether these factors are responsible for the development of compression-induced autophagy. RESULTS: Our results indicated that rat NP cells activated autophagy in response to the same strong apoptotic stimuli that triggered apoptosis by compression. Autophagy and apoptosis were interconnected and coordinated in rat NP cells exposed to compression stimuli. Compression-induced autophagy was closely related to intracellular ROS production. CONCLUSIONS: Enhanced degradation of damaged components of NP cells by autophagy may be a crucial survival response against mechanical overload, and extensive autophagy may trigger autophagic cell death. Regulating autophagy and reducing the generation of intracellular ROS may retard IVD degeneration. SN - 1522-9653 UR - https://www.unboundmedicine.com/medline/citation/24120490/Autophagy_is_activated_in_compression_induced_cell_degeneration_and_is_mediated_by_reactive_oxygen_species_in_nucleus_pulposus_cells_exposed_to_compression_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1063-4584(13)00973-4 DB - PRIME DP - Unbound Medicine ER -