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J Biomed Transl Res. 2017 Dec;18(4):130-135. English. Original Article.
Kil KM , Jung SH , Jeon IS , Cho BK , Park JK , Park KJ , Kim YM , Choi JK .
Department of Biochemistry, College of Medicine, Chungbuk National University, Cheongju 28644, Korea.
Department of Orthopaedic Surgery, College of Medicine, Chungbuk National University, Cheongju 28644, Korea.

Adhesive capsulitis of the shoulder is a common cause of pain that occurs during shoulder movement, thereby restricting shoulder rotation in clinical practice. Although most patients respond to pain relief treatment (NSAID or corticosteroids) by improving their range of motion, it remains poorly understood without any definitive treatment algorithm. In addition to immune cells, synoviocytes, chondrocytes and osteoblasts in the joint are known to produce pro-inflammatory mediators such as reactive oxygen species (ROS), inflammatory cytokines and lipid mediators, presumably contributing to the pathogenesis of osteoarthritis (OA) and adhesive capsulitis. Although inflammation and also fibrosis are proposed to be the basic pathological changes of a frozen shoulder, there is a lack of information regarding the downstream targets of the pro-inflammatory ROS signaling pathway in the synoviocytes and also how these ROS targets are modulated at the transcription level by a corticosteroid - dexamethasone. In this study, we used human fibroblast like synoviocytes (HFLS) to characterize the signaling targets of ROS by employing a human DNA microarray tool and studied the role of dexamethasone in this process. Our data suggest that several genes such as FOS, FOSB and NFkBIZ, which are known to be involved in pro- or anti- inflammation response, are modulated at the transcription level by ROS and dexamethasone.

Copyright © 2019. Korean Association of Medical Journal Editors.