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Mitochondrial function is altered in articular chondrocytes of an endemic osteoarthritis, Kashin-Beck disease.
Osteoarthritis Cartilage. 2010 Sep; 18(9):1218-26.OC

Abstract

OBJECTIVE

Kashin-Beck disease (KBD) is an endemic degenerative osteoarthritis (OA) associated with extracellular matrix degradation and chondrocyte necrosis in the articular and growth plate cartilage. The role of mitochondria in degenerative diseases is widely recognized but its function in KBD is unknown. The aim of this investigation was to evaluate mitochondrial function to understand the mitochondria-mediated caspase activation and apoptosis in adult KBD chondrocytes.

METHODS

Mitochondrial function was evaluated by analyzing the activities of respiratory chain enzyme complexes and citrate synthase (CS), intracellular adenosine triphosphate (ATP) contents, as well as changes in mitochondrial membrane potential (DeltaPsim). Apoptotic cell death was evaluated by analyzing the cytochrome c release from mitochondria to the cytosol, caspase-9 and 3 activities, and the apoptosis rate of KBD articular chondrocytes.

RESULTS

Activities of complexes II, III, IV and V were reduced in KBD articular chondrocytes compared with cells from normal controls. However, the mitochondrial mass was increased in KBD samples. Cultured KBD chondrocytes had a reduction of cellular ATP levels and contained a higher proportion of cells with de-energized mitochondria. Mitochondrial cytochrome c release and activation of caspase-9 and 3 were also observed. The percentages of positive apoptotic chondrocytes from the KBD patient group stained by Hoechst nuclear stain and Annexin V/PI for flow cytometry exhibited higher levels than that of the healthy controls.

CONCLUSION

These findings suggest the involvement of mitochondrial function and apoptotic cell death in the pathophysiology of KBD. The dysfunction of the mitochondria may play an important role in KBD articular chondrocytes apoptosis.

Authors+Show Affiliations

Faculty of Public Health, College of Medicine, Key Laboratory of Environment and Gene Related Diseases of Ministry Education, Xi'an Jiaotong University, Xi'an, Shaanxi, PR China.No 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

20650322

Citation

Liu, J T., et al. "Mitochondrial Function Is Altered in Articular Chondrocytes of an Endemic Osteoarthritis, Kashin-Beck Disease." Osteoarthritis and Cartilage, vol. 18, no. 9, 2010, pp. 1218-26.
Liu JT, Guo X, Ma WJ, et al. Mitochondrial function is altered in articular chondrocytes of an endemic osteoarthritis, Kashin-Beck disease. Osteoarthr Cartil. 2010;18(9):1218-26.
Liu, J. T., Guo, X., Ma, W. J., Zhang, Y. G., Xu, P., Yao, J. F., & Bai, Y. D. (2010). Mitochondrial function is altered in articular chondrocytes of an endemic osteoarthritis, Kashin-Beck disease. Osteoarthritis and Cartilage, 18(9), 1218-26. https://doi.org/10.1016/j.joca.2010.07.003
Liu JT, et al. Mitochondrial Function Is Altered in Articular Chondrocytes of an Endemic Osteoarthritis, Kashin-Beck Disease. Osteoarthr Cartil. 2010;18(9):1218-26. PubMed PMID: 20650322.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial function is altered in articular chondrocytes of an endemic osteoarthritis, Kashin-Beck disease. AU - Liu,J T, AU - Guo,X, AU - Ma,W J, AU - Zhang,Y G, AU - Xu,P, AU - Yao,J F, AU - Bai,Y D, Y1 - 2010/08/01/ PY - 2010/02/27/received PY - 2010/07/08/revised PY - 2010/07/14/accepted PY - 2010/7/24/entrez PY - 2010/7/24/pubmed PY - 2011/2/25/medline SP - 1218 EP - 26 JF - Osteoarthritis and cartilage JO - Osteoarthr. Cartil. VL - 18 IS - 9 N2 - OBJECTIVE: Kashin-Beck disease (KBD) is an endemic degenerative osteoarthritis (OA) associated with extracellular matrix degradation and chondrocyte necrosis in the articular and growth plate cartilage. The role of mitochondria in degenerative diseases is widely recognized but its function in KBD is unknown. The aim of this investigation was to evaluate mitochondrial function to understand the mitochondria-mediated caspase activation and apoptosis in adult KBD chondrocytes. METHODS: Mitochondrial function was evaluated by analyzing the activities of respiratory chain enzyme complexes and citrate synthase (CS), intracellular adenosine triphosphate (ATP) contents, as well as changes in mitochondrial membrane potential (DeltaPsim). Apoptotic cell death was evaluated by analyzing the cytochrome c release from mitochondria to the cytosol, caspase-9 and 3 activities, and the apoptosis rate of KBD articular chondrocytes. RESULTS: Activities of complexes II, III, IV and V were reduced in KBD articular chondrocytes compared with cells from normal controls. However, the mitochondrial mass was increased in KBD samples. Cultured KBD chondrocytes had a reduction of cellular ATP levels and contained a higher proportion of cells with de-energized mitochondria. Mitochondrial cytochrome c release and activation of caspase-9 and 3 were also observed. The percentages of positive apoptotic chondrocytes from the KBD patient group stained by Hoechst nuclear stain and Annexin V/PI for flow cytometry exhibited higher levels than that of the healthy controls. CONCLUSION: These findings suggest the involvement of mitochondrial function and apoptotic cell death in the pathophysiology of KBD. The dysfunction of the mitochondria may play an important role in KBD articular chondrocytes apoptosis. SN - 1522-9653 UR - https://www.unboundmedicine.com/medline/citation/20650322/Mitochondrial_function_is_altered_in_articular_chondrocytes_of_an_endemic_osteoarthritis_Kashin_Beck_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1063-4584(10)00228-1 DB - PRIME DP - Unbound Medicine ER -