Int J Med Sci
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The treatment of bone loss due to periodontitis has posed a great challenge for physicians for decades. Therefore, it is of extraordinary significance to identify an effective regeneration scheme for alveolar bone. This study aimed to investigate long non-coding RNA (lncRNA) small nucleolar RNA host gene 5 (SNHG5) whether sponges microRNA-23b-3p (miR-23b-3p) to achieve the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs). ⋯ Dual luciferase report and RNA pulldown assay verified that miR-23b-3p is a regulatory target of SNHG5 and that Runx2 is a gene target of miR-23b-3p. In brief, the results demonstrate that SNHG5 promotes the osteogenic differentiation of hPDLSCs by regulating the miR-23b-3p/Runx2 axis. Our study provides novel mechanistic insights into the critical role of lncRNA SNHG5 as a miR-23b-3p sponge to regulate Runx2 expression in hPDLSCs and may serve as a potential therapeutics target for periodontitis.
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Atherosclerosis is a chronic, inflammatory disease characterized by a lipid-driven infiltration of inflammatory cells in large and medium arteries and is considered to be a major underlying cause of cardiovascular diseases. Cuproptosis, a novel form of cell death, is highly linked to mitochondrial metabolism and mediated by protein lipoylation. However, the clinical implication of cuproptosis-related genes (CRGs) in atherosclerosis remains unclear. ⋯ The area under the curve (AUC) of SLC31A1, SLC31A2 and SOD1 performed well for the diagnostic validation in the two datasets. In conclusion, the cuproptosis-related gene signature could serve as a potential diagnostic biomarker for atherosclerosis and may offer novel insights into the treatment of cardiovascular diseases. Based on the hub genes, a competing endogenous RNA (ceRNA) network of lncRNA-miRNA-mRNA and a transcription factor regulation network were ultimately constructed to explore the possible regulatory mechanism in atherosclerosis.
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With the increased incidence of age-related and lifestyle-related diseases, chronic wounds are sweeping the world, where recent studies reveal that dysfunction of fibroblast plays an indispensable role. Endogenous electric field (EF) generated by skin wound disrupting an epithelial layer has been used as an alternative clinical treatment in chronic wound by modulating cellular behaviours, including fibroblasts transdifferentiation. Although many molecules and signaling pathways have been reported associated with fibroblasts transdifferentiation, studies investigating how the electric field affects the cellular pathways have been limited. ⋯ Furthermore, we found that electric field activated RhoA signaling pathways activity. Y-27632, a RhoA inhibitor, which was used to treat fibroblasts, resulted in reduced transdifferentiation. The connection between electric field and RhoA signaling pathways is likely to be significant in modulating fibroblast transdifferentiation in acute injury and tissue remodeling, which provides an innovative idea for the molecular mechanism of EF in promoting chronic wound healing.
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Background: Mantle cell lymphoma (MCL) is a heterogeneous disease belonging to non-Hodgkin's lymphoma. In recent years, the morbidity rate of MCL is ascending, and the prognosis remains unfavorable. Ubiquitin-specific proteases14 (USP14) has been evidenced to be engaged in the process of malignant tumors. ⋯ Interference of USP14 suppressed MCL cell viability, potentiated cell cycle arrest, apoptosis, and ibrutinib sensitivity. This process might be achieved by USP14 deubiquitination through enhancing XPO1 stability. Conclusion: USP14 can promote the malignant progression and ibrutinib sensitivity of MCL by stabilizing XPO1.
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Background: Aspergillus fumigatus-specific immunoglobulin G (Af-sIgG) has been applied to diagnose allergic bronchopulmonary aspergillosis, a hypersensitivity reaction to the colonization of the fungus in the lower airways. In the upper airways, it has been reported to be involved in allergic fungal rhinosinusitis and local fungal rhinosinusitis. However, in primary chronic rhinosinusitis (CRS), a more common upper airway disease, the role of Af-sIgG remains unclear. ⋯ Conclusions: We suggest that the serum Af-sIgG level is a practical marker to detect T2 inflammation and the surgical outcome of primary CRS. By applying this feasible test, we may be able to achieve optimal treatment for every individual with primary CRS. This study may provide physicians with a reference for future clinical applications in dealing with primary CRS.