How does temperature play a role in the storage of extracellular vesicles?

Extracellular vesicles (EVs) contain specific proteins, lipids, and nucleic acids that can be passed to other cells as signal molecules to alter their function. However, there are many problems and challenges in the conversion and clinical application of EVs. Storage and protection of EVs is one of the issues that need further research. To adapt to potential clinical applications, this type of problem must be solved. This review summarizes the storage practices of EVs in recent years, and explains the impact of temperature on the quality and stability of EVs during storage based on current research, and explains the potential mechanisms involved in this effect as much as possible.

Abnormal expression of key genes and proteins in the canonical Wnt/ß-catenin pathway of articular cartilage in a rat model of exercise-induced osteoarthritis.

To investigate the molecular pathogenesis of the canonical Wnt/ß-catenin pathway in exercise-induced osteoarthritis (OA), 30 male healthy Sprague Dawley rats were divided into three groups (control, normal exercise­induced OA and injured exercise­induced OA groups) in order to establish the exercise­induced OA rat model. The mRNA and protein expression levels of Runx­2, BMP­2, Ctnnb1, Sox­9, collagen Ⅱ, Mmp­13, Wnt­3a and ß­catenin in chondrocytes were detected by reverse transcription­quantitative polymerase chain reaction, western blotting and immunohistochemical staining. The mRNA levels of Runx­2, BMP­2 and Ctnnb1 were upregulated in the normal exercise­induced OA and injured exercise­induced OA groups; while Runx­2 and BMP­2 were upregulated in the injured exercise­induced OA group when compared with the normal exercise­induced OA group. The protein levels of Mmp­13, Wnt­3a and ß­catenin were increased and collagen Ⅱ was reduced in the normal exercise­induced OA and injured exercise­induced OA groups. Ctnnb1, Wnt­3a and ß­catenin, which are key genes and proteins in the canonical Wnt/ß­catenin pathway, were abnormally expressed in chondrocytes of the exercise­induced OA rat model. Ctnnb1, ß­catenin and Wnt­3a were suggested to participate in the pathogenesis of exercise­induced OA by abnormally activating the Wnt/ß­catenin pathway during physical exercise due to excessive pressure. The results of the present study may provide an improved understanding of the pathogenesis of exercise-induced OA.