The aim of this study was to determine whether supplementation with vitamin D during eight weeks of high-intensity training influences muscle power and aerobic performance in young soccer players. A total of 25 athletes were divided into two groups: the supplemented group (GS; n = 12; vitamin D 20,000 IU, twice a week) and the non-supplemented group (GN; n = 13). A set of measurements, including sprint tests, explosive power test, maximal oxygen uptake (VO2max), and serum 25(OH)D concentration, were obtained before (T1) and after (T2) the intervention. A significant group x time interaction was found in the 25(OH)D serum levels (p = 0.002; ES = 0.36, large). A significant improvement in VO2max was found in the TG (p = 0.0004) and the GS (p = 0.031). Moreover, a positive correlation between 25(OH)D and VO2max (R = 0.4192, p = 0.0024) was calculated. The explosive power tests revealed insignificant time interactions in the average 10-jump height and average 10-jump power (p = 0.07, ES = 0.13; p = 0.10, ES = 0.11, respectively). A statistically insignificant trend was observed only in the group-by-time interaction for the sprint of 10 m (p = 0.05; ES = 0.15, large). The present study provides evidence that vitamin D supplementation has a positive but trivial impact on the explosive power and locomotor skills of young soccer players, but could significantly affect their aerobic performance.

Background/Objectives: Osteoarthritis (OA) is the most common degenerative and chronic joint disease and is a leading cause of pain and disability in adults worldwide. The SRY-related HMG box (SOX) family transcription factors (TFs) play a crucial role during the pathogenesis of OA; however, their exact mechanisms remain unexplored. The aim of our study was to conduct a bioinformatics analysis of the common interactions of SOX-5, SOX-9, and SOX-11 with other proteins, as well as their role in OA pathogenesis. Methods:SOX5, SOX9, and SOX11 mRNA expression levels in articular cartilage with subchondral bone and synovium from knee OA patients were assessed using the qPCR method. The study group consisted of thirty-one patients (n = 31). Total RNA was isolated from the articular cartilage with subchondral bone and synovium from the affected and unaffected area of the knee joint. Results: Our results revealed a regulatory network between SOX-5, SOX-9, and SOX-11, and various proteins involved in the pathogenesis of knee OA and their collective interactions, which are involved in the regulation of cartilage extracellular matrix (ECM) organization, response to stimulus, regulation of gene expression, inflammatory response, cartilage condensation, and ossification in chondrocytes. Higher expression levels of SOX5, SOX9, and SOX11 mRNA were noted in OA-affected articular cartilage with subchondral bone compared to control tissue (p = 0.00015, p = 0.0024 and p > 0.05, respectively, Mann–Whitney U-test). All studied genes demonstrated elevated mRNA expression levels in the articular cartilage with subchondral bone from stage 4 patients than those with stage 3 (p > 0.05; Mann–Whitney U-test). Lower SOX5, SOX9, and SOX11 mRNA expression levels were found in OA-affected synovium compared to the control tissue (p = 0.0003, p > 0.05 and p = 0.0007, respectively, Mann–Whitney U-test). Decreased SOX9 mRNA expression levels in synovium were noted in patients with stage 4 disease than those with stage 3; however, SOX5 and SOX11 mRNA expression levels were higher in patients with stage 4 (p > 0.05; Mann–Whitney U-test). Conclusions: The results of our research show that the studied SOX TFs play a role in the development of OA, contributing to the formation of pathological changes not only in the articular cartilage, but also in the synovial membrane. The changes in the SOX5, SOX9, and SOX11 mRNA expression levels in the articular cartilage with subchondral bone and synovium may serve as potential molecular diagnostic biomarkers for detecting OA and could indicate the progression of this disease; however, our observations require further investigation.

Background/Objectives: Osteoarthritis (OA) is a very common degenerative joint disease that has a significant negative impact on patients’ lives and which can lead to functional limitations and disability. Matrix metalloproteinase 13 (MMP-13) is a key enzyme responsible for the degenerative changes in cartilage occurring during the pathogenesis of OA. This cohort study analyzed the differences in the expression level of MMP13 mRNA in articular cartilage with subchondral bone and in the synovium of patients with OA, according to the disease stage, in order to develop potential markers for OA progression, as well as for the degree of pain perception, in order to discover a molecular biomarker related to pain. Methods: In thirty-one patients (n = 31), the expression level of the studied gene was assessed in the affected and unaffected areas of the knee joint using the qPCR method. Statistical analysis was performed using the Mann–Whitney U test, the Kruskal–Wallis test, and Spearman’s rank correlation coefficient. Results: A significantly higher expression level of MMP13 mRNA was noticed in the OA-affected articular cartilage with subchondral bone compared to the control tissue (p = 0.027, Mann–Whitney U test). The expression level of MMP13 mRNA was higher in patients with stage 4 knee OA than in those with stage 3, but the difference in MMP13 mRNA expression level was statistically insignificant (p > 0.05, Mann–Whitney U test). A higher MMP13 mRNA expression level was noticed in the OA-affected synovium compared to the control tissue (median RQ: 0.068 and 0.037, respectively), but these differences were not significant (p > 0.05, Mann–Whitney U test). A significantly higher MMP13 mRNA expression level was observed in the synovium of stage 4 knee OA patients compared to stage 3 patients (p = 0.015, Mann–Whitney U test). There was no significant difference in the expression level of MMP13 mRNA between both tissues, i.e., the articular cartilage with subchondral bone and the synovium from the stage 3 group and the control tissue (p > 0.05, Mann–Whitney U test); however, a significant difference was found between these tissues in stage 4 and in the control tissue (p = 0.014, Mann–Whitney U test). Conclusions: The results of our pilot study indicated the diagnostic potential of MMP13 mRNA and proved its role in the development and progression of OA. Further studies are needed to verify the potential utility of MMP13 mRNA in the development of molecularly targeted therapy for patients with OA.

Background: Osteoarthritis (OA) patients experience poorer quality of life due to persistent symptoms and chronic pain. Unfortunately, the molecular basis of OA development is poorly understood, thus posing a major challenge for therapeutic interventions. The aim of this study was to compare the expression of genes encoding key cartilage proteins in OA-affected tissue from the relatively preserved lateral compartment of the knee joint in relation to knee OA advancement stage. This study focuses on molecular changes in individual areas of the knee, which may be important for the use of partial endoprostheses in patients. Methods: This study included 31 patients with primary knee OA. OA-affected tissues (medial compartment of the knee joint) and tissues from the relatively preserved lateral compartment were collected from each patient. Gene expression was assessed by real-time polymerase chain reaction (PCR). A protein–protein interaction network and functional visualization were prepared. Results: Compared with the relatively preserved lateral compartment, the more severely OA-affected medial compartment demonstrated significantly higher COL1A1 mRNA expression in articular cartilage (p = 0.0045; Holm-adjusted p = 0.0269) and significantly higher ACAN mRNA expression in synovial tissue (p = 0.0091; Holm-adjusted p = 0.0458). In an exploratory subgroup analysis, patients with hypertension showed significantly higher COL1A1 mRNA expression in cartilage from the more severely OA-affected medial compartment than in the relatively preserved lateral compartment (p = 0.00054). The verified proteins were found to be associated with proteins involved in the cartilage development. Based on The Gene Expression Omnibus (GEO) database, late-OA chondrocytes presented higher ACAN and COL1A1, and lower collagen type II (COL2A1) mRNA expression than early-OA ones. In the synovium, late-OA tissue from the relatively preserved lateral compartment showed lower ACAN and higher COL1A1 mRNA expression than early-OA tissue. Conclusions: Numerous molecular changes are associated with OA. Cartilage and synovial membranes demonstrated similar changes in ACAN mRNA expression, whereas COL1A1 and COL2A1 displayed divergent expression patterns. The observed differences in gene expression depended on the part of tissue studied, biological features of patients and presence of comorbidities.