Water-based lubricants provide lubrication of rubbing surfaces in many technical, biological, and physiological applications. The structure of hydrated ion layers adsorbed on solid surfaces that determine the lubricating properties of aqueous lubricants is thought to be invariable in hydration lubrication. However, we prove that the ion surface coverage dictates the roughness of the hydration layer and its lubricating properties, especially under subnanometer confinement. We characterize different hydration layer structures on surfaces lubricated by aqueous trivalent electrolytes. Two superlubrication regimes are observed with friction coefficients of 10 −4 and 10 −3 , depending on the structure and thickness of the hydration layer. Each regime exhibits a distinct energy dissipation pathway and a different dependence to the hydration layer structure. Our analysis supports the idea of an intimate relationship between the dynamic structure of a boundary lubricant film and its tribological properties and offers a framework to study such relationship at the molecular level.
Epigenetic modulations lead to changes in gene expression, including DNA methylation, histone modifications, and noncoding RNAs. In recent years, epigenetic modifications have been related to the pathogenesis of different types of cancer, cardiovascular disease, and other diseases. Emerging evidence indicates that DNA methylation could be associated with ischemic stroke (IS) and plays a role in pathological progression, but the underlying mechanism has not yet been fully understood. In this study, we used human methylation 850K BeadChip to analyze the differences in gene methylation status in the peripheral blood samples from two groups (3 IS patients vs. 3 healthy controls). According to their bioinformatics profiling, we found 278 genes with significantly different methylation levels. Seven genes with the most significant methylation modifications were validated in two expanded groups (100 IS patients vs. 100 healthy controls). The CAMTA1 gene had significantly different methylation changes in patients compared to the controls. To understand the CAMTA1 function in stroke, we generated CAMTA1 knockout in SH-SY5Y cells. RNA seq results in CAMTA1 knockout cells revealed the pathways and gene set enrichments involved in cellular proliferation and cell cycle. Furthermore, a series of experiments demonstrated that in the oxygen-glucose deprivation/re-oxygenation (OGD/R) model system, the expression of cyclin D1, an essential regulator of cell cycle progression, was increased in SH-SY5Y CAMTA1 KO cells. Increasing evidence demonstrated that ischemic stress could inappropriately raise cyclin D1 levels in mature neurons. However, the molecular signals leading to an increased cyclin D1 level are unclear. Our findings demonstrate for the first time that the CAMTA1 gene could regulate cyclin D1 expression and implicate their role in strokes.
ATP binding cassette subfamily A1 (ABCA1) is a key protein in the formation of mature high density lipoprotein (HDL), which plays a crucial role in atherosclerosis. Accumulating evidence has shown that the expression levels of the ABCA1 gene are upregulated in ischemic stroke (IS) patients. However, the mechanism remains elusive. We hypothesized that DNA methylation and SNPs of ABCA1 gene promoter affect the expression levels of ABCA1 gene and involve in the pathological mechanism of IS. 100 patients with IS and 100 healthy controls were enrolled in the present study. Initially, the mRNA expression levels of ABCA1 gene were examined by qPCR and the methylation levels was detected by MethyTarget sequencing. Then, rs1800976, rs1800977, rs2246298, rs2437817, rs2740483, rs539621172 in promoter region of ABCA1 gene were selected for genotyping. Finally, the relationship between the methylation of ABCA1 gene and gene expression was verified by constructing THP-1 foam cell model. The mRNA expression levels of ABCA1 gene in the IS group were significantly higher than those in controls (P<0.05). 17 CpG sites in the promoter of ABCA1 gene were analyzed and the DNA methylation levels of CpG1, CpG7 and CpG15 sites in IS group was significantly lower than control group (P<0.05). Rs2740483, rs1800977 and rs2437817 were significantly correlated with CpG1. Rs1800977 was significantly correlated with CpG3. In summary, DNA methylation and rs2740483, rs1800977, rs2437817 of ABCA1 gene promoter affect the expression levels of ABCA1 gene, change the clearance rate of intracellular lipids, and participate in the pathogenesis of IS.
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