Molecular Biology Reports最新文献

Multiple sclerosis (MS) is a chronic immune-mediated disorder of the central nervous system marked by demyelination, inflammation, and progressive neuronal damage. Current immunotherapies reduce relapse frequency but fail to stop silent progression driven by microglial activation or to promote effective remyelination. Mesenchymal stem cells (MSCs) have shown therapeutic promise; however, their clinical use is restricted by issues of survival, distribution, and large-scale production. Increasing evidence indicates that MSC benefits are primarily mediated by their secretome, especially exosomes, nanosized vesicles that carry proteins, lipids, and nucleic acids that modulate immune activity and enhance neuroregeneration. In preclinical models, MSC-derived exosomes suppress pro-inflammatory microglia, increase anti-inflammatory signaling, and stimulate oligodendrocyte maturation and myelin repair. These vesicles can cross the blood-brain barrier, exhibit low immunogenicity, and function as cell-free therapeutics. Early clinical findings in non-neurological disorders confirm their safety, while intranasal administration offers a practical delivery route. Collectively, these insights highlight exosomes as a promising next-generation therapy capable of addressing both inflammation and neurodegeneration in multiple sclerosis.

Dental stem cells (DSCs) have emerged as valuable tools in regenerative medicine due to their ability to differentiate into various cell types, including adipocytes. Although their adipogenic potential is generally described as modest or lower compared with mesenchymal stem cells from other sources, DSCs remain useful in vitro models for studying the mechanisms underlying adipose tissue formation. This review highlights recent advances in the epigenetic regulation of adipogenesis, including insights from histone modifications, particularly H3K9, which we contextualize within the broader landscape of epigenetic regulation in DSCs and other mesenchymal stem cells (MSCs). Additionally, the effects of epigenetic drugs are analyzed, and differences in adipogenic commitment among various types of DSCs are discussed. These findings underscore their importance as models for designing therapies targeting metabolic diseases.

Background: Endometriosis (EMs) is a chronic enigmatic gynecological disorder which pathogenesis have not been fully elucidated. Exosomes have been proven to participate in endometriosis. However, the role of exosomes in the pathogenesis of EMs remains poorly defined.

Methods: Exosomes were isolated from cyst fluid of EMs patients and pelvic fluid of non-EMs patients, and characterized by transmission electron microscopy, nanoparticle tracking analysis and western blot. Exosomal miRNAs were performed by small RNA sequencing. Q-PCR and cell function were performed to identify the relationship between exosomal miRNAs and endometriosis. Dual luciferase reporter assay, cell transfection, Q-PCR, Western blotting and CCK8 assays, Transwell assays and Boyden assays were conducted to explore the regulatory effects of exosomal miRNA on EMs pathogenesis in vitro using primary human endometrial stromal cells (HESCs) derived from endometriotic lesions.

Results: Compare with non-EMs group, there are 118 miRNAs were up-regulated and 40 miRNAs were down-regulated in CF group, meanwhile 22 miRNAs were up-regulated and 32 miRNAs were down-regulated in PF group. Q-PCR verified that miR-125b-5p, miR-328-3p, miR-125a-5p, miR-30e-3p were significant down-regulated, whereas miR-3141, miR-223-3p, miR-142-5p, miR-1246 were significant up-regulated in EMs patients. ROC analysis indicated that miR-125b-5p (AUC = 0.925, p < 0.001) was highly correlated with EMs pathogenesis. Dual luciferase reporter assay results demonstrated miR-125b-5p directly targeted VEGF gene. MiR-125b-5p suppressed endometrial stromal cells proliferation, migration and invasion by regulating the Phosphatidylinositol 3-Kinase (PI3K) /Protein Kinase B (AKT) signaling pathway.

Conclusion: Exosomal miR-125b-5p was highly correlated with EMs, and it regulates the PI3K/Akt signaling pathways through VEGF to inhibit endometrial stromal cells proliferation, migration and invasion, acting as an important suppressing miRNA in endometriosis pathogenesis.

Background: Patients undergoing cardiac surgery frequently suffer impaired myocardial redox protection during cardiopulmonary bypass (CPB), with elderly patients facing higher complication risks. We investigated the redox-protective effects of blood versus del Nido cardioplegia on systemic redox homeostasis, stratified by age, in patients undergoing coronary bypass and isolated valve surgery.

Methods: Systemic redox biomarkers were assessed with immunochemical and spectrophotometric methods in patients stratified by cardioplegia type (blood vs. del Nido) and age (< 60 vs. ≥60 years). Redox biomarkers such as MnSOD, catalase, total thiol, PCO, AOPP, LOOH, GPxA, and AGE were analyzed in blood samples of postoperative CPB patients (n = 60).

Results: MnSOD levels were significantly higher with blood cardioplegia, indicating increased mitochondrial oxidative stress, whereas lower levels in the del Nido group suggested improved redox balance. Catalase activity appeared higher in the del Nido group, potentially influenced by outliers. Total thiol levels varied significantly among younger patients: those receiving blood cardioplegia had higher thiol concentrations, suggesting a more robust antioxidant buffer. No significant differences were observed regarding PCO, AOPP, LOOH, GPxA, or AGE between groups.

Conclusions: This analysis highlights MnSOD as the most reliable biomarker for differentiating cardioplegia strategies. Lower MnSOD levels in the del Nido group support its superior redox-protective effects, which are particularly relevant for reducing surgical complications in elderly patients undergoing cardiac surgery.