Paper Title
The Effect Of Estrogen Receptor-Βand Tensile Stress On Tendinopathy

De Quervain’s disease and tendonitis are common tendinopathies of the hand.They are musculoskeletal disorders caused by repetitive hand posture and motion and considered as overuse syndromes. These diseases are all female dominance. Association seemed to exist between the disorders. We previously showed that estrogen receptor-β (ER-β) expression was higher in patients with de Quervain’s disease. The expression of ERs may be associated with female-dominant diseases. However, how estrogen modulates the pathogenesis of diseases was not clear. Alteration of hormone levels and external mechanical stress may mutually affect each other during disease pathogenesis. To study the effect of the factors on diseases, we examined the ER-β expression from patients with de Quervain’s disease using immunohistochemistry staining. A collagenase-induced tendinopathy model of rat was set up. The tissues were examined during disease progression. Furthermore, a cyclic stretching culture system was used to evaluate the additive effect of tensile stress on tissues. Our results showed that the expression of ER-β was higher in patients with de Quervain’s disease and rats with tendonitis, and that the degree of expression was related to the disease severity, so as the ratio of ER-β and ER-α. After 24 hours cyclic stretching, the mechanic strain caused the morphology of tenocytes changed. The immuohistochemical staining and TUNEL assay revealed increased levels ofIL-1β¸ER-βand apoptosis. The collagen fiber alignment of tissues changed after stretching. As seen in cells, an increase expression ofTLR-4, ER-β, MMP9 and apoptosis was seen. However, the inflammation and apoptosis were alleviatedusing the same stretching conditionin tissues from a oophorectomy model of rat. Our results showed that the altered expression of ER-βmay affect the regulation of estrogen signaling pathway and result in the inflammation and apoptosis in tenocytes. External consistent mechanic stress exacerbated the disease progression. It may provide a potential target for the treatment of tendinopathy.