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Oxidative damage induces apoptosis and promotes calcification in disc cartilage endplate cell through ROS/MAPK/NF-κB pathway: Implications for disc degeneration.
Biochem Biophys Res Commun 2019; 516(3):1026-1032BB

Abstract

Cartilage endplate (CEP) cell calcification and apoptosis play a vital role in the intervertebral disc degeneration (IVDD). Oxidative stress is a key factor in inducing programmed cell death and cartilage calcification. However, the cell death and calcification of cartilage endplate cells under oxidative stress have never been described. The present study investigated the apoptosis and calcification in the cartilage endplate cell under oxidative stress induced by H2O2 to understand the underlying mechanism of IVDD. The cartilage endplate cells isolated from human lumbar discs were subjected to different concentrations of H2O2 for various time periods. The cell viability was determined by CCK-8 assay, whereas Western blot, immunofluorescence, and Alcian blue, Alizarin red, and Von Kossa staining evaluated the apoptosis and calcification. The level of mitochondria-specific reactive oxygen species (ROS) was quantified with an oxygen radical-sensitive probe-MitoSOX. The potential signaling pathways were investigated by Western blot after the addition of N-acetyl-l-cysteine (NAC). We found that the oxidative stress induced by H2O2 increased the apoptosis and subsequently the calcification in the cartilage endplate cells through the ROS/p38/ERK/p65 pathway. The apoptosis and the calcification of the cartilage endplate cells induced by H2O2 can be abolished by NAC. These results suggested that regulating the apoptosis and the calcification in the cartilage endplate cells under oxidative stress should be advantageous for the survival of cells and might delay the process of disc degeneration.

Authors+Show Affiliations

Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China; Department of Joint and Bone Disease, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai, 200120, China. Electronic address: hycmed@163.com.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China. Electronic address: lljunspine@163.com.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, School of Medicine, 150 Jimo Road, Shanghai 200120, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28342871

Citation

Han, Yingchao, et al. "Oxidative Damage Induces Apoptosis and Promotes Calcification in Disc Cartilage Endplate Cell Through ROS/MAPK/NF-κB Pathway: Implications for Disc Degeneration." Biochemical and Biophysical Research Communications, vol. 516, no. 3, 2019, pp. 1026-1032.
Han Y, Li X, Yan M, et al. Oxidative damage induces apoptosis and promotes calcification in disc cartilage endplate cell through ROS/MAPK/NF-κB pathway: Implications for disc degeneration. Biochem Biophys Res Commun. 2019;516(3):1026-1032.
Han, Y., Li, X., Yan, M., Yang, M., Wang, S., Pan, J., ... Tan, J. (2019). Oxidative damage induces apoptosis and promotes calcification in disc cartilage endplate cell through ROS/MAPK/NF-κB pathway: Implications for disc degeneration. Biochemical and Biophysical Research Communications, 516(3), pp. 1026-1032. doi:10.1016/j.bbrc.2017.03.111.
Han Y, et al. Oxidative Damage Induces Apoptosis and Promotes Calcification in Disc Cartilage Endplate Cell Through ROS/MAPK/NF-κB Pathway: Implications for Disc Degeneration. Biochem Biophys Res Commun. 2019 Aug 27;516(3):1026-1032. PubMed PMID: 28342871.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative damage induces apoptosis and promotes calcification in disc cartilage endplate cell through ROS/MAPK/NF-κB pathway: Implications for disc degeneration. AU - Han,Yingchao, AU - Li,Xinhua, AU - Yan,Meijun, AU - Yang,Mingjie, AU - Wang,Shanjin, AU - Pan,Jie, AU - Li,Lijun, AU - Tan,Jun, Y1 - 2017/03/23/ PY - 2017/02/09/received PY - 2017/03/21/accepted PY - 2017/3/28/pubmed PY - 2017/3/28/medline PY - 2017/3/27/entrez KW - Apoptosis KW - Calcification KW - Cartilage endplate (CEP) KW - Intervertebral disc degeneration (IVDD) KW - Oxidative stress KW - Reactive oxygen species (ROS) SP - 1026 EP - 1032 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 516 IS - 3 N2 - Cartilage endplate (CEP) cell calcification and apoptosis play a vital role in the intervertebral disc degeneration (IVDD). Oxidative stress is a key factor in inducing programmed cell death and cartilage calcification. However, the cell death and calcification of cartilage endplate cells under oxidative stress have never been described. The present study investigated the apoptosis and calcification in the cartilage endplate cell under oxidative stress induced by H2O2 to understand the underlying mechanism of IVDD. The cartilage endplate cells isolated from human lumbar discs were subjected to different concentrations of H2O2 for various time periods. The cell viability was determined by CCK-8 assay, whereas Western blot, immunofluorescence, and Alcian blue, Alizarin red, and Von Kossa staining evaluated the apoptosis and calcification. The level of mitochondria-specific reactive oxygen species (ROS) was quantified with an oxygen radical-sensitive probe-MitoSOX. The potential signaling pathways were investigated by Western blot after the addition of N-acetyl-l-cysteine (NAC). We found that the oxidative stress induced by H2O2 increased the apoptosis and subsequently the calcification in the cartilage endplate cells through the ROS/p38/ERK/p65 pathway. The apoptosis and the calcification of the cartilage endplate cells induced by H2O2 can be abolished by NAC. These results suggested that regulating the apoptosis and the calcification in the cartilage endplate cells under oxidative stress should be advantageous for the survival of cells and might delay the process of disc degeneration. SN - 1090-2104 UR - https://www.unboundmedicine.com/medline/citation/28342871/Oxidative_damage_induces_apoptosis_and_promotes_calcification_in_disc_cartilage_endplate_cell_through_ROS/MAPK/NF_κB_pathway:_Implications_for_disc_degeneration_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(17)30578-8 DB - PRIME DP - Unbound Medicine ER -