The current first-line treatment for repairing cartilage defects in clinical practice is the creation of microfractures (MF) to stimulate the release of mesenchymal stem cells (MSCs); however, this method has many limitations. Recent studies have found that MSC-derived extracellular vesicles (MSC-EVs) play an important role in tissue regeneration. This study aimed to verify whether MSC-EVs promote cartilage damage repair mediated by MFs and to explore the repair mechanisms. In vitro experiments showed that human umbilical cord Wharton’s jelly MSC-EVs (hWJMSC-EVs) promoted the vitality of chondrocytes and the proliferation and differentiation ability of bone marrow-derived MSCs. This was mainly because hWJMSC-EVs carry integrin beta-1 (ITGB1), and cartilage and bone marrow-derived MSCs overexpress ITGB1 after absorbing EVs, thereby activating the transforming growth factor-β/Smad2/3 axis. In a rabbit knee joint model of osteochondral defect repair, the injection of different concentrations of hWJMSC-EVs into the joint cavity showed that a concentration of 50 µg/ml significantly improved the formation of transparent cartilage after MF surgery. Extraction of regenerated cartilage revealed that the changes in ITGB1, transforming growth factor-β, and Smad2/3 were directly proportional to the repair of regenerated cartilage. In summary, this study showed that hWJMSC-EVs promoted cartilage repair after MF surgery. Graphical abstract

The establishment of a tree shrew model for systemic lupus erythematosus (SLE) provides a new method to evaluate the pathogenesis of autoimmune diseases. Eighty tree shrews were randomly divided into four groups receiving either an intraperitoneal injection of pristane, lipopolysaccharide (LPS), or pristane and LPS, or no injection. Three weeks after injection, the SLE model tree shrews were divided into the model group and the treatment group. Tree shrews in the treatment group and the normal control group were infused with umbilical cord mesenchymal stem cells (UC-MSCs). The cells were labeled with DiR. Two weeks after transplantation, three groups of tree shrews were analyzed for urine protein, serum antinuclear antibodies and antiphospholipid, and inflammatory cytokine antibody microarray detection. The heart, liver, spleen, lung, and kidney were collected from the three groups and subjected to hematoxylin and eosin (HE) staining and detection of renal immune complex deposition. HE staining indicated pathology in the model group. Red fluorescence revealed immune complex deposition in the kidneys from the model group. The combined intraperitoneal injection of pristane and LPS is the best way to induce SLE pathological changes. The pathological changes improved after UC-MSC treatment.

Background. Systemic lupus erythematosus (SLE) is a multisystem disease that is characterized by the appearance of serum autoantibodies. No effective treatment for SLE currently exists.Methods. We used human umbilical cord mesenchymal stem cell (H-UC-MSC) transplantation to treat B6.Fas mice.Results. After four rounds of cell transplantation, we observed a statistically significant decrease in the levels of mouse anti-nuclear, anti-histone, and anti-double-stranded DNA antibodies in transplanted mice compared with controls. The percentage of CD4⁺CD25⁺Foxp3⁺T cells in mouse peripheral blood significantly increased after H-UC-MSC transplantation.Conclusions. The results showed that H-UC-MSCs could repair lesions in B6.Fas mice such that all of the relevant disease indicators in B6.Fas mice were restored to the levels observed in normal C57BL/6 mice.

Previous studies have confirmed that ascorbic acid (AA) can promote cartilage repair and improve cartilage differentiation in bone marrow mesenchymal stem cells. However, the use of microfracture (MFX) combined with AA to repair cartilage damage has not been studied. This study established a rabbit animal model and treated cartilage injury with different concentrations of AA combined with MFX. Macroscopic observations, histological analysis, immunohistochemical analysis and reverse transcription quantitative polymerase chain reaction analysis of TGF-β, AKT/Nrf2, and VEGF mRNA expression were performed. The results showed that intra-articular injection of AA had a positive effect on cartilage repair mediated by microfractures. Moreover, 10 mg/ml AA was the most effective at promoting cartilage repair mediated by microfractures. Intra-articular injection of AA promoted the synthesis of type II collagen and the formation of glycosaminoglycans by downregulating the mRNA expression of TGF-β and VEGF. In summary, this study confirmed that AA could promote cartilage repair after MFX surgery.

This study aimed to investigate the relationship between immunosenescence and osteoarthritis (OA) and analyze its potential clinical implications. Thus, we conducted transcriptome sequencing by collecting clinical meniscus (Aging_meniscus:Control_meniscus = 3:7) and cartilage tissues (Aging_cartilage:Control_cartilage = 2:6). Meanwhile, immune-related genes (IRGs) and aging-related genes (ARGs) were included in this research. The differentially expressed genes (DEGs) between Aging_meniscus and Control_meniscus as well as Aging_cartilage and Control_cartilage were analyzed by differential analysis, respectively. Then, differentially expressed IRGs (DEIRGs) were generated by crossing DEG with IRGs. Similarly, differentially expressed ARGs (DEARGs) were achieved by intersecting DEG and ARGs. To obtain genes simultaneously associated with immune and aging in both meniscus and cartilage samples, biomarkers were screened out by crossing share.IRGs and share.ARGs overlapped by DEIRGs1 and DEIRGs2 as well as DEARGs1 and DEARGs2, respectively. In addition, the biomarkers’ functions were analyzed by gene set enrichment analysis (GSEA). To detect the regulatory mechanism, a miRNA-mRNA-transcription factors (TFs) regulatory network and a X2K network were constructed. Moreover, disease association analysis and potential small molecule drugs for biomarkers were also performed to further reveal the possible role of biomarkers for OA. Then, 3 biomarkers, namely Insulin-like Growth Factor 1 Receptor (IGF1R), Interleukin 7 receptor (IL7R) and Leptin receptor (LEPR), were selected out through the intersection of 14 share.IRGs and 4 share.ARGs. And they were all enriched in ‘ribosome’ from both meniscus and cartilage samples, and had complex regulatory networks. In all, the expression of IGF1R was markedly up-regulated in OA (P < 0.05). Eventually, mecasermin could stably bind to IGF1R and simvastatin could stably bind to LEPR. It suggested that mecasermin and simvastatin may exhibit significant clinical potential in treating immunosenescence-related OA.

Previous studies have confirmed that scald injuries can lead to disturbances in hepatic lipid metabolism, and bone marrow-derived mesenchymal stem cells (B