Association between the platelet/high-density lipoprotein cholesterol ratio and depression: A cross-sectional analysis in United States adults.

BACKGROUND: The primary objective of this study was to elucidate the relationship between the platelet/high-density lipoprotein cholesterol ratio (PHR) and the risk of depression in adults in the US. METHODS: We conducted a cross-sectional study using data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2016. Depression was assessed using the PHQ-9 questionnaire. Weighted multivariable logistic regression models and restricted cubic spline (RCS) models were used to study the relationship between PHR and the risk of depression. Subgroup and interaction analyses were performed to further understand these associations. RESULTS: A total of 21,454 participants were included in this study. After full adjustment, PHR was significantly positively correlated with depression (OR = 1.33, 95%CI: 1.03-1.73). When PHR was converted into a categorical variable based on quartiles (Q1-Q4), the highest quartile of PHR was associated with an increased risk of depression compared to the lowest reference group (OR = 1.22, 95%CI: 1.01-1.48). There was a linear dose-response relationship between PHR and the risk of depression (P-non-linear = 0.8038). The association remained significant in several subgroup analyses. However, the interaction test showed that none of the stratified variables were significant (all P for interaction >0.05). LIMITATION: Using self-assessment scales and inability to assess causality. CONCLUSION: This population-based cross-sectional study elucidated that PHR is significantly associated with an increased prevalence of depression in adults in the US.

M2-like tumor-associated macrophages transmit exosomal miR-27b-3p and maintain glioblastoma stem-like cell properties.

There is growing evidence supporting the implications of exosomes-shuttled microRNAs (miRs) in the phenotypes of glioblastoma stem cells (GSCs), whilst the role of exosomal miR-27b-3p remains to be established. Herein, the aim of this study was to investigate the effect of M2 tumor-associated macrophage (TAM)-derived exosomal miR-27b-3p on the function of GSCs. Clinical glioblastoma (GBM) specimens were obtained and GSCs and M2-TAMs were isolated by fluorescence-activated cell sorting (FACS), and exosomes were separated from M2-TAMs. It was observed that M2-TAM-derived exosomes promoted the stem-like properties of GSCs. Gain- and loss- of function assays were then conducted to explore the effects of exosomal miR-27b-3p and the miR-27b-3p/MLL4/PRDM1 axis on GSC phenotypes. A xenograft tumor model of GBM was further established for in vivo substantiation. Inhibition of miR-27b-3p in M2-TAMs reduced exosomal miR-27b-3p transferred into GSCs and consequently diminished GSC viability in vitro and tumor-promoting effects of GSCs in vivo. The interaction among miR-27b-3p, mixed linked leukemia 4 (MLL4), positive regulatory domain I (PRDM1) was validated by dual-luciferase and ChIP assays. MLL4 positively regulated PRDM1 expression by inducing methylation in the PRDM1 enhancer region and ultimately reduced IL-33 expression. miR-27b-3p targeted MLL4/PRDM1 to activate IL-33 and maintain the stem-like function of GSCs. In conclusion, our study elucidated that M2-TAM-derived exosomal miR-27b-3p enhanced the tumorigenicity of GSCs through the MLL4/PRDM1/IL-33 axis.

microRNA-27a-3p delivered by extracellular vesicles from glioblastoma cells induces M2 macrophage polarization via the EZH1/KDM3A/CTGF axis.

Glioblastoma (GBM) cell-derived extracellular vesicles (EVs) have been demonstrated to modulate tumor microenvironment. In the present study, we attempted to discuss the role of hsa-microRNA-27a-3p (miR-27a-3p) delivered by GBM-EVs in M2 macrophage polarization. The isolated GBM-EVs were co-cultured with macrophages. After co-culture under normoxia/hypoxia, the effect of EV-derived hsa-miR-27a-3p on GBM cell biological processes was analyzed. Additionally, the target genes of hsa-miR-27a-3p were predicted. Moreover, the binding of enhancer of zeste homologue 1 (EZH1) to lysine-specific demethylase 3A (KDM3A) promoter region and the interaction between KDM3A and connective tissue growth factor (CTGF) were analyzed. GBM mouse models were established to verify the functions of EV-derived hsa-miR-27a-3p in vivo. We found increased hsa-miR-27a-3p in GBM tissues as well as GBM-EVs, which induced M2 polarization, thus promoting proliferative, migrative and invasive potentials of GBM cells. hsa-miR-27a-3p targeted EZH1 and promoted KDM3A expression to elevate the CTGF expression. GBM-EV-delivered hsa-miR-27a-3p promoted the KDM3A-upregulated CTGF by downregulating EZH1, thereby promoting M2 macrophage polarization and development of GBM in vivo. We demonstrated that EV-derived hsa-miR-27a-3p may promote M2 macrophage polarization to induce GBM.

[Expression of hsa-miR-20a in human glioma tissues and its effect on the proliferation of human glioma cells in vitro].

OBJECTIVE: To investigate miR-20a expression in human glioma and normal brain tissues and its effect on the proliferation of glioma cells in vitro. METHODS: The expression of miR-20a was detected in human normal brain tissues and glioma tissues by real-time RT-PCR. miR-20a mimics were synthesized and transfected into U251 cells via liposome, and the cell proliferation were detected using MTT assay and flow cytometry. RESULTS: The glioma tissues showed significantly up-regulated expression of miR-20a compared with normal brain tissues (P=0.035). The expression level of miR-20a was higher in high-grade than in low-grade gliomas. miR-20a mimics significantly enhanced the proliferation of U251 cells and the percentage of S-phase cells. CONCLUSION: miR-20a shows potent effect in promoting the growth of glioma cells, suggesting its important role in the pathogenesis of human glioma.