Project description:We compared genes from tissue of patients with adhesive capsulitis (AC) with those having surgery for shoulder instability to determine potential biomarkers specific to AC through transcriptomic analysis. Our results presented increased expression of PDGFB, COL18A1 and MMP9 in patients with AC, while TNFA expression was reduced.
Project description:Adhesive capsulitis (AC) affects 2–5% of the population worldwide. Patients with severe AC fail to regain a complete range of movement and experience years of shoulder pain. Unfortunately, the underlying mechanism of severe AC remains unclear. Here, we performed an integrated transcriptomic and metabolomic data analysis of serum and tissue samples from patients with severe AC, mild AC, and healthy controls. Pathways related to muscle development and myogenesis positively correlated with severe AC progression. Further, we identified an arginine-citrulline gene-compound network that may play a central role in severe AC. Comparing differentially regulated metabolites from tissue and serum, two phospholipids were recognized as potential serum markers for severe AC. In conclusion, this is the first comprehensive integrated -omics study on severe AC and provides insights into genes and compounds of the arginine-citrulline metabolic pathway that may be potential therapeutic targets for treating AC.
Project description:Osteoarthritis (OA) is a disease impacting the synovial joint complex, yet transcriptional changes specific to shoulder OA remain underexplored. This study aims to profile transcriptomic changes in periarticular tissues from patients undergoing shoulder replacement for OA. By correlating these profiles with QuickDASH scores—a validated measure of worsening shoulder function—this research seeks to understand the gene expression changes associated with clinical decline. Capsular tissue biopsies from shoulder OA patients were compared with those from a control group undergoing shoulder stabilization for recurrent instability. This investigation forms part of a larger transcriptomic analysis of painful shoulder conditions which will address the current gap in knowledge regarding the molecular and genetic underpinnings of shoulder OA, rotator cuff tears and cuff-tear arthropathy.
Project description:Bulk transcriptomic data of shoulder capsule fibroblasts isolated from frozen shoulder co-cultured with Dexamethasone (DEX) or LPS treated monocyte-derived macrophages (MDM), which were isolated from blood cones and stimulated with M-CSF, for 72 hours. The stimulated MDMs have been characterised as MerTKhigh(DEX) and MerTKlow(LPS). Unstimulated, DEX and LPS stimulated MDM were co-cultured with ex vivo shoulder capsule-derived fibroblasts from patients with frozen shoulder. Fibroblasts were then FACS isolated and RNA-sequencing analysis performed. As an additional control ex vivo fibroblasts were also profiled without co-culture (stimulation=”none”).
Project description:We utilize bulk RNA-seq to profile the mRNA expression in day 3 and day 14 post-implantation of SD rat abdminal wall treated with adhesive or non-adhesive implants
Project description: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 non-coding RNAs, microRNAs (miRNAs) 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-26 KO and wild type (WT) mice were investigated using a frozen shoulder model. The range of motion of the shoulder, histopathological analysis such as synovitis, and fibrosis related-genes 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 range of motion compared with WT mice at each point, and histological changes were notably 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.
Project description:We harvested the blood samples from rotator cuff tear patients with and without shoulder stiffness.Then, circulating exosomes were harvested, and the miRNAs content was analyzed with an aim to idenfity differentially expressed miRNAs.