Jeng-Long Hsieh

1Department of Nursing, Chung Hwa University of Medical Technology, Taiwan



Biography

Jeng-Long had completed her PhD from the Institute of Basic Medical Science, National Cheng Kung University. She is presently the Dean of the College of Nursing, Chung Hwa University of Medical Technology, a historic school that fostered many medical personnel in the south of Taiwan. She has published more than twenty-five research articles in reputed journals and has been serving as a reviewer of many repute journals.

Abstract

Musculoskeletal disorders represent a global threat to healthy ageing, and are ranked as the second most common cause of disability. Significantly contributing to the global disability burden associated with the musculoskeletal system are inflammatory arthritis and tendinopathy. Alteration of hormone levels affects both disease progression. A higher risk of rheumatoid arthritis (RA) was associated with the tendinopathy. We previously showed that estrogen receptor-β (ER-β) expression was higher in patients with tendinopathy and it resulted in apoptosis. The expression of ERs may be associated with RA. To examine if the expression of ER-β are correlated with disease activity of RA and the molecular mechanisms underlying the regulation of ERs. Synovial tissue from patients with RA was collected, the tissues were examined by immunochemical staining. A collagenase-induced arthritis (CIA) model of rat was established. The expression of ER-β and cytokines, chemokines of RA synovial fibroblast (RASF) was examined by real-time PCR and ELISA. A lentiviral vectors that encoded ER-β short-hairpin RNA (shRNA) was intraarticularly injected into the rats. Immunohistochemical staining revealed higher expression of ER-β in synovial tissues from patients with RA and rats with CIA compared with that in synovial tissue from patients with osteoarthritis and normal rats. The quantitative analysis showed that the expression of ER-β, IL-6, CCL5, and c-met of RASF was higher than that of control counterparts. ER-β shRNAs inhibited ER-β expression, which alleviate the disease manifestation.

Our study revealed that ER-β regulated the inflammatory response in RA. Local inhibition of ER-β might have therapeutic effect of RA.