MicroRNA‐26a deficiency attenuates the severity of frozen shoulder in a mouse immobilization model.

The main pathogenesis of the frozen shoulder is thought to be the inflammation of the intra‐articular synovium and subsequent fibrosis of the shoulder joint capsule. However, the molecular pathogenesis of the frozen shoulder is still unknown. A class of noncoding RNAs, microRNAs contribute to various diseases including musculoskeletal diseases. MicroRNA‐26a (miR‐26a) has been reported to be associated with fibrosis in several organs. This study aims to reveal the role of miR‐26a on fibrosis in the shoulder capsule using a frozen shoulder model in miR‐26a deficient (miR‐26a KO) mice. MiR‐26a KO and wild‐type (WT) mice were investigated using a frozen shoulder model. The range of motion (ROM) of the shoulder, histopathological changes such as synovitis, and fibrosis‐related gene expression in the model mice were evaluated to determine the role of miR‐26a. In WT mice, both inflammatory cell infiltration and thickening of the inferior shoulder joint capsule were observed after 1 week of immobilization, and this thickening further progressed over the subsequent 6 weeks. However, the immobilized shoulder in miR‐26a KO mice consistently exhibited significantly better ROM compared with WT mice at 1 and 6 weeks, and histological changes were significantly less severe. The expression of inflammation‐ and fibrosis‐related genes was decreased in the miR‐26a KO mice compared with WT mice at 1 and 6 weeks. Together, miR‐26a deficiency attenuated the severity of frozen shoulder in the immobilization model mouse. The present study suggests that miR‐26a has the potential to be a target miRNA for therapeutic approach to frozen shoulder. [ABSTRACT FROM AUTHOR]