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Identification of differently expressed genes and pathways in cartilage of Kashin-Beck disease using microarray / 中国地方病学杂志
Chinese Journal of Endemiology ; (6): 159-163, 2013.
Article in Chinese | WPRIM | ID: wpr-643258
ABSTRACT
Objective To identify differently expressed genes and pathways between Kashin-Beck disease (KBD) cartilage and healthy cartilage,and to explore the mechanism of articular cartilage lesions of KBD.Methods Cartilage specimens were collected from 9 patients with KBD and 9 healthy controls.Total RNA was extracted from cartilage specimens,and transcribed into cDNA.KBD and control groups were labeled by Cy3 and Cy5,respectively.Agilent genome-wide microarray was applied to compare the expression profile of KBD cartilage and healthy cartilage.The microarray data was analyzed by single gene and pathway expression analysis to identify differently expressed genes and pathways between KBD and healthy controls.Results ①Tweenty nine genes were significantly up-regulated in KBD group (averaged ratio =6.68 + 1.98,P < 0.05),mainly involved in apoptosis,metabolism,extracellular matrix,cytoskeleton and cell movement.Additionally,extracellular matrix-related FBLN1 gene was down-regulated in KBD group(ratio =0.14 + 0.06,P < 0.05).②Five apoptosis and 6 hypoxia-related pathways presented higher expression levels in KBD compared to healthy controls(all P< 0.05).Conclusions We find significant expression differences of apoptosis and hypoxia-related genes and pathways between KBD cartilages and healthy cartilages,suggesting that hypoxia might contribute to chondrocytes apoptosis of KBD.Further studies may be needed to investigate the relationship between hypoxia and articular cartilage lesions of KBD.

Full text: Available Index: WPRIM (Western Pacific) Type of study: Diagnostic study Language: Chinese Journal: Chinese Journal of Endemiology Year: 2013 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Type of study: Diagnostic study Language: Chinese Journal: Chinese Journal of Endemiology Year: 2013 Type: Article