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3-morpholinosydnonimine (SIN-1)-induced oxidative stress leads to necrosis in hypertrophic chondrocytes in vitro.
Biomed Pharmacother. 2018 Oct; 106:1696-1704.BP

Abstract

Chondrocyte is targeted for disruption in Osteoarthritis (OA) and Kashin-Beck Disease (KBD), and chondrocyte death in cartilage may contribute to the progression of OA and KBD. Oxidative stress leads to increased risk for OA. Previous work in our laboratory implicates oxidative stress as a potential mediator in children with KBD. While these studies suggest a role for oxidative stress in the modulation of OA and KBD, the direct effects of reactive oxygen species/reactive nitrogen species (ROS/RNS) on the stability of this domain remain unclear. Here, we demonstrate that oxidative stress, as induced through treatment with 3-morpholinosydnonimine (SIN-1), a spontaneous ROS/RNS generator, decreased the cell viability in hypertrophic chondrocytes in a dose- and time- dependent manner. SIN-1 induced necrosis in hypertrophic chondrocytes, whereas triggered apoptosis in non-hypertrophic cells of non-differentiated ATDC5 cells and C28/I2 cells. Ultrastructural analysis of hypertrophic chondrocyte treated with SIN-1 revealed morphological changes, such as plasma membrane breakdown, generalized swelling of the cytoplasm and organelles, even to disappearance. Moreover, SIN-1 induced chondronecrosis in the deep zone of engineered cartilage tissue, such as cell-free vacancy and "red ghost" cells. Overall, we demonstrate for the first time that oxidative stress, as induced through exogenous ROS/RNS, leads to necrosis in hypertrophic chondrocytes. Oxidative stress-mediated necrotic cell death contributes to chondronecrosis in the deep zone of cartilage in both OA and KBD.

Authors+Show Affiliations

Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, 710061, Shaanxi, PR China; Graduate Students Teaching Experiment Center, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, PR China.Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, 710061, Shaanxi, PR China.Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, 710061, Shaanxi, PR China.Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, 710061, Shaanxi, PR China.Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, 710061, Shaanxi, PR China.Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, 710061, Shaanxi, PR China.Research Division, HSS Research Institute, Hospital for Special Surgery, and Weill Cornell Medical College, 535 East 70th Street, New York, New York, 10021, USA.Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, 710061, Shaanxi, PR China. Electronic address: jixiang46@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30119244

Citation

He, Ying, et al. "3-morpholinosydnonimine (SIN-1)-induced Oxidative Stress Leads to Necrosis in Hypertrophic Chondrocytes in Vitro." Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, vol. 106, 2018, pp. 1696-1704.
He Y, Zhang Y, Zhang D, et al. 3-morpholinosydnonimine (SIN-1)-induced oxidative stress leads to necrosis in hypertrophic chondrocytes in vitro. Biomed Pharmacother. 2018;106:1696-1704.
He, Y., Zhang, Y., Zhang, D., Zhang, M., Wang, M., Jiang, Z., Otero, M., & Chen, J. (2018). 3-morpholinosydnonimine (SIN-1)-induced oxidative stress leads to necrosis in hypertrophic chondrocytes in vitro. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 106, 1696-1704. https://doi.org/10.1016/j.biopha.2018.07.128
He Y, et al. 3-morpholinosydnonimine (SIN-1)-induced Oxidative Stress Leads to Necrosis in Hypertrophic Chondrocytes in Vitro. Biomed Pharmacother. 2018;106:1696-1704. PubMed PMID: 30119244.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 3-morpholinosydnonimine (SIN-1)-induced oxidative stress leads to necrosis in hypertrophic chondrocytes in vitro. AU - He,Ying, AU - Zhang,Ying, AU - Zhang,Dan, AU - Zhang,Meng, AU - Wang,Mengying, AU - Jiang,Zhuocheng, AU - Otero,Miguel, AU - Chen,Jinghong, Y1 - 2018/07/30/ PY - 2018/05/11/received PY - 2018/07/05/revised PY - 2018/07/24/accepted PY - 2018/8/19/pubmed PY - 2018/12/12/medline PY - 2018/8/19/entrez KW - Apoptosis KW - Hypertrophic chondrocytes KW - Necrosis KW - Oxidative stress SP - 1696 EP - 1704 JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JO - Biomed. Pharmacother. VL - 106 N2 - Chondrocyte is targeted for disruption in Osteoarthritis (OA) and Kashin-Beck Disease (KBD), and chondrocyte death in cartilage may contribute to the progression of OA and KBD. Oxidative stress leads to increased risk for OA. Previous work in our laboratory implicates oxidative stress as a potential mediator in children with KBD. While these studies suggest a role for oxidative stress in the modulation of OA and KBD, the direct effects of reactive oxygen species/reactive nitrogen species (ROS/RNS) on the stability of this domain remain unclear. Here, we demonstrate that oxidative stress, as induced through treatment with 3-morpholinosydnonimine (SIN-1), a spontaneous ROS/RNS generator, decreased the cell viability in hypertrophic chondrocytes in a dose- and time- dependent manner. SIN-1 induced necrosis in hypertrophic chondrocytes, whereas triggered apoptosis in non-hypertrophic cells of non-differentiated ATDC5 cells and C28/I2 cells. Ultrastructural analysis of hypertrophic chondrocyte treated with SIN-1 revealed morphological changes, such as plasma membrane breakdown, generalized swelling of the cytoplasm and organelles, even to disappearance. Moreover, SIN-1 induced chondronecrosis in the deep zone of engineered cartilage tissue, such as cell-free vacancy and "red ghost" cells. Overall, we demonstrate for the first time that oxidative stress, as induced through exogenous ROS/RNS, leads to necrosis in hypertrophic chondrocytes. Oxidative stress-mediated necrotic cell death contributes to chondronecrosis in the deep zone of cartilage in both OA and KBD. SN - 1950-6007 UR - https://www.unboundmedicine.com/medline/citation/30119244/3_morpholinosydnonimine__SIN_1__induced_oxidative_stress_leads_to_necrosis_in_hypertrophic_chondrocytes_in_vitro_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0753-3322(18)33209-8 DB - PRIME DP - Unbound Medicine ER -