Comparative analysis of gene expression profiles between the normal human cartilage and the one with endemic osteoarthritis

Guo³

et al. 2012

Sci. China Life Sci.

In this paper, we present the first evidence of differences in the mitochondria-related gene expression profiles of adult articular cartilage derived from patients with Kashin-Beck disease and normal controls. The expression of 705 mitochondria-related genes was analyzed by mitochondria-related gene expression analysis and ingenuity pathways analysis. Mitochondria-related gene expression analysis identified 9 up-regulated genes in Kashin-Beck disease based on their average expression ratio. Three canonical pathways involved in oxidative phosphorylation, apoptosis signaling and pyruvate metabolism were identified, which indicate the involvement of mitochondrial dysfunction in the pathogenesis of Kashin-Beck disease. Kashin-Beck disease, microarray, mitochondrial dysfunction, IPA analysis Citation:Li C Y, Wang W Z, Guo X, et al. Pathways related to mitochondrial dysfunction in cartilage of endemic osteoarthritis patients in China.

Section: Discussionsupporting

confidence: 68%

mentioning

confidence: 94%

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

Li¹,

Guo³

et al. 2012

Sci. China Life Sci.

“…As the observation of the higher expression of TNF-a, VEGF, TGF-b and IL-1 in KBD cartilage [22], inflammation may be both a primary event in KBD and/or a secondary event in the disease. The KBD is characterized by chondrocyte apoptosis and pathological changes after cartilage necrosis, inflammation response maybe or may activate the up-stream of the chondrocytes apoptosis.…”

Section: Inflammatory Pathways Activated In Kbdmentioning

confidence: 99%

Role of inflammation in the process of clinical Kashin-Beck disease: latest findings and interpretations

Han

et al. 2015

Inflamm. Res.

Kashin-Beck disease (KBD), a particular type of osteoarthritis (OA), and an endemic disease with articular cartilage damage and chondrocytes apoptosis, can affect many joints, and the most commonly affected joints are the knee, ankle, and hand. KBD has traditionally been classified as a non-inflammatory OA. However, recent studies have shown that inflammation has played an important role in the development of KBD. Nowadays, clinical KBD is not only an endemic disease, but also a combined result of many other non-endemic factors, which contains age, altered biomechanics, joint trauma and secondary OA. The characteristics of the developmental joint failure of advanced KBD, because of the biochemical and mechanical processes, are tightly linked with the interaction of joint damage and its immune response, as well as the subsequent state of chronic inflammation leading to KBD progression. In this review, we focus on the epidemiology, pathology, imaging, cytokines and transduction pathways investigating the association of inflammation with KBD; meanwhile, a wide range of data will be discussed to elicit our current hypotheses considering the role of inflammation and immune activation in KBD development.

“…A number of studies have analyzed the differentially expressed genes of peripheral blood to identify marker genes for early diagnosis of diseases including cancer, coronary disease and OA (8)(9)(10)(11)(12). With regard to KBD, in prior studies differentially expressed genes in cartilage and peripheral blood have been screened using microarrays (1,7,13). Although single gene expression analyses are important for authenticating the related target genes of KBD and OA, KBD is a gene-environment interactional disease; therefore, gene network and pathway analyses may prove more comprehensive and effective for the early diagnosis and therapy of KBD and OA, as compared with single gene analyses.…”

Section: Introductionmentioning

confidence: 99%

Comparative analysis of signaling pathways in peripheral blood from patients with Kashin-Beck disease and osteoarthritis

Ning

Experimental and Therapeutic Medicine

et al. 2016

Abstract. The aim of the present study was to investigate the early diagnostic biomarkers of Kashin-Beck disease (KBD), and to compare the common signaling pathways of peripheral mononuclear cells between patients with KBD and those with osteoarthritis (OA). A total of 20 and 12 peripheral blood samples were separately collected from KBD patients and normal control subjects, respectively, in an endemic area according to the diagnosis criteria. Total RNAs were extracted and gene expression levels were determined using an Agilent whole genome expression microarrays. The gene expression data of OA were obtained from GEO published database. Significant different pathways between KBD and OA were analyzed using Ingenuity Pathway Analysis software. A total of 82 differentially expressed genes, 51 significant different signaling pathways and five significant biological functions were identified in KBD patient samples, while 89, 50 and five significantly different genes, pathways and functions were identified in OA. Nine common significant pathways and five common differentially expressed genes were identified between the KBD and OA. Nine common significant pathways and five common differentially expressed genes were found between the two diseases. The present results suggest that there are similarities in vascular microcirculation, immunoreactions and cell apoptosis between KBD and OA, which may contribute to the early diagnosis and pathogenetic study of KBD.