Pathways related to mitochondrial dysfunction in cartilage of endemic osteoarthritis patients in China

Li, ChunYan Y.; Wang, WeiZhuo Z.; Guo, Xiong; zhang, Feng; WeiJuan, J.; Zhang, YinGang G.; Li, YouFen F.; Bai, Yidong

doi:10.1007/s11427-012-4418-4

Cited by 9 publications

(6 citation statements)

References 27 publications

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“…It was indicated that the dysfunction of the mitochondria play an important role in KBD chondrocyte damages in our recent study, and T-2 toxin, a possible pathogenic factor of KBD, increases Bax protein production and induces chondrocyte apoptosis [19] , [20] , [23] , [24] . The present data from analyses of cell viability, mitochondrial function and mitochondria- mediated apoptosis reveal that T-2 toxin caused insults to human chondrocytes via a mitochondrial pathway.…”

Section: Discussionmentioning

confidence: 99%

The Role of Mitochondria in T-2 Toxin-Induced Human Chondrocytes Apoptosis

et al. 2014

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T-2 toxin, a mycotoxin produced by Fusarium species, has been shown to cause diverse toxic effects in animals and is also a possible pathogenic factor of Kashin–Beck disease (KBD). The role of mitochondria in KBD is recognized in our recent research. The aim of this study was to evaluate the role of mitochondria in T-2 toxin-induced human chondrocytes apoptosis to understand the pathogenesis of KBD. T-2 toxin decreased chondrocytes viabilities in concentration- and time-dependent manners. Exposure to T-2 toxin can reduce activities of mitochondrial complexes III, IV and V, ΔΨm and the cellular ATP, while intracellular ROS increased following treatment with T-2 toxin. Furthermore, mitochondrial cytochrome c release, caspase-9 and 3 activation and chondrocytes apoptosis were also obviously observed. Interestingly, Selenium (Se) can partly block T-2 toxin -induced mitochondria dysfunction, oxidative damage and chondrocytes apoptosis. These results suggest that the effect of T-2 toxin on human chondrocytes apoptosis may be mediated by a mitochondrial pathway, which is highly consistent with the chondrocytes changes in KBD.

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Section: Discussionmentioning

confidence: 99%

The Role of Mitochondria in T-2 Toxin-Induced Human Chondrocytes Apoptosis

et al. 2014

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“…Here, we reported that expressions of certain genes related to the function of mitochondria were altered in RA patients. Notably, the relevant genes, which include the ATP6, SCO2 , CYTB, DN1, COX1, ANT1 , are mainly function in oxidative phosphorylation, whereas dysfunction in oxidative phosphorylation related genes is closely related to the systemic juvenile idiopathic arthritis and endemic osteoarthritis [40], [41]. This largely indicates that both RA and OA can be classified as mitochondrial disorder.…”

Section: Discussionmentioning

confidence: 99%

Functional Annotation of Rheumatoid Arthritis and Osteoarthritis Associated Genes by Integrative Genome-Wide Gene Expression Profiling Analysis

Xiao

Peng

et al. 2014

PLoS ONE

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BackgroundRheumatoid arthritis (RA) and osteoarthritis (OA) are two major types of joint diseases that share multiple common symptoms. However, their pathological mechanism remains largely unknown. The aim of our study is to identify RA and OA related-genes and gain an insight into the underlying genetic basis of these diseases.MethodsWe collected 11 whole genome-wide expression profiling datasets from RA and OA cohorts and performed a meta-analysis to comprehensively investigate their expression signatures. This method can avoid some pitfalls of single dataset analyses.Results and ConclusionWe found that several biological pathways (i.e., the immunity, inflammation and apoptosis related pathways) are commonly involved in the development of both RA and OA. Whereas several other pathways (i.e., vasopressin-related pathway, regulation of autophagy, endocytosis, calcium transport and endoplasmic reticulum stress related pathways) present significant difference between RA and OA. This study provides novel insights into the molecular mechanisms underlying this disease, thereby aiding the diagnosis and treatment of the disease.

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“…applied to analyze the gene expression profile data of the KBD cartilage vs the healthy cartilage. This analysis found that the apoptosis-, hypoxia-and mitochondria-related pathways were significantly up-regulated in the KBD patients compared to the healthy controls 58,59 . For instance, the pathways related to various types of the intracellular stress, including the growth factor withdrawal, the DNA damage, the unfolding stresses in the endoplasmic reticulum, and the death receptor stimulation were affected by the disease, in addition to the adaptive immunity-associated gene expressions in the peripheral blood mononuclear cells 60 .…”

Section: The Gene Expression Profilingmentioning

confidence: 91%

Recent advances in the research of an endemic osteochondropathy in China: Kashin-Beck disease

Guo¹,

Ma²,

Zhang³

et al. 2014

Osteoarthritis and Cartilage

169

130

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Kashin-Beck disease (KBD) is an endemic chronic osteochondral disease, which has a high prevalence and morbidity in the Eastern Siberia of Russia, and in the broad diagonal, northern-east to southern-west belt in China and North Korea. In 1990's, it was estimated that in China 1-3 million people had some degree of symptoms of the disease, although even higher estimates have been presented. In China, the extensive prevalence peaked in the late 1950's, but since then, in contrast to the global trend of the osteoarthritis (OA), the number of cases has been dramatically falling. Up to 2013, there are 0.64 millions patients with the KBD and 1.16 millions at risk in 377 counties of 13 provinces or autonomous regions. This is obviously thanks to the preventive efforts carried out, which include providing millions of people with dietary supplements and clean water, as well as relocation of whole villages in China. However, relatively little is known about the molecular mechanisms behind the cartilage damage, the genetic and the environmental risk factors, and the rationale of the preventive effects. During the last decade, new data on a cellular and molecular level has begun to accumulate, which hopefully will uncover the grounds of the disease.

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Pathways related to mitochondrial dysfunction in cartilage of endemic osteoarthritis patients in China

Cited by 9 publications

References 27 publications

The Role of Mitochondria in T-2 Toxin-Induced Human Chondrocytes Apoptosis

The Role of Mitochondria in T-2 Toxin-Induced Human Chondrocytes Apoptosis

Functional Annotation of Rheumatoid Arthritis and Osteoarthritis Associated Genes by Integrative Genome-Wide Gene Expression Profiling Analysis

Recent advances in the research of an endemic osteochondropathy in China: Kashin-Beck disease

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