ß-1,6-Glucan From Pleurotus eryngii Modulates the Immunity and Gut Microbiota.

Polysaccharides from Pleurotus eryngii exhibit a variety of biological activities. Here, we obtained a homogeneous branched ß-1,6-glucan (APEP-A-b) from the fruiting bodies of P. eryngii and investigated its effect on immunity and gut microbiota. Our results showed that APEP-A-b significantly increases splenic lymphocyte proliferation, NK cell activity and phagocytic capacity of peritoneal cavity phagocytes. Furthermore, we found that the proportion of CD4+ and CD8+ T cells in lamina propria are significantly increased upon APEP-A-b treatment. Additionally, APEP-A-b supplementation demonstrated pronounced changes in microbiota reflected in promotion of relative abundances of species in the Lachnospiraceae and Rikenellaceae families. Consistently, APEP-A-b significantly increased the concentration of acetic and butyric acid in cecum contents. Overall, our results suggest that ß-1,6-glucan from P. eryngii might enhance immunity by modulating microbiota. These results are important for the processing and product development of P. eryngii derived polysaccharides.

LncRNA-MIAT promotes neural cell autophagy and apoptosis in ischemic stroke by up-regulating REDD1.

BACKGROUND: Ischemic stroke (IS) accounts for 80% of stroke incidence, which has an impact on the life quality of patients. Long non-coding RNA (LncRNA), a class of non-coding transcripts greater than 200 nucleotidesin length, has been extensively studied in cerebrovascular diseases. Myocardial infarction associated transcript (MIAT) is highly expressed in nervous system. Therefore this study aims to explore the role of LncRNA MIAT in IS and to clarify its underlying mechanism, providing therapeutic value for the treatment of IS. METHODS: The neurological function of rats was evaluated by neurological deficit score. Triphenyltetrazolium chloride (TTC) staining was used to detect infarct area in brain tissues. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine the expression of MIAT. Western blotting was used to detect the expressions of REDD1, p-mTOR, autophagy-related proteins LC3 and p62, and apoptotic-related proteins Bax, cleaved-caspase3, Bcl-2. Flow cytometry was applied to examine neuronal cell apoptosis. RNA pull-down and RIP assay was used to verify the binding of MIAT and REDD1. The level of REDD1 ubiquitination was detected by ubiquitination and Co-immunoprecipitation (Co-IP) assay. RESULTS: The expressions of MIAT and REDD1 were increased in IS rats and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced PC12 cell injury. After interference with si-MIAT, the results of flow cytometry showed that the rate of apoptosis was reduced. Western blotting results showed that the expression of LC3II/LC3I, Bax, and cleaved-caspase3 was decreased, while the expression of p-mTOR, p62, and Bcl-2 was increased. RNA pull-down and RIP assay found the binding relationship between MIAT and REDD1, and interference with si-MIAT down-regulated the expression of REDD1. The level of REDD1 ubiquitination was increased and the expression of REDD1 was decreased after interference with si-MIAT in PC12 cells. Co-IP results showed that interference with si-MIAT enhanced the binding ability of CUL4A-DDB1 and REDD1. CONCLUSION: Altogether, MIAT promotes autophagy and apoptosis of neural cells and aggravates IS by up-regulating the expression of REDD1.

Circular RNA circ_DROSHA alleviates the neural damage in a cell model of temporal lobe epilepsy through regulating miR-106b-5p/MEF2C axis.

Temporal lobe epilepsy (TLE) is the most prevalent form of acquired epilepsy. Circular RNAs (circRNAs) have recently been highlighted as important regulators in TLE. Nevertheless, the role and mechanism of circRNA Drosha ribonuclease III (circ_DROSHA) in TLE pathogenesis are still unknown. Magnesium-free extracellular solution was used to establish the TLE cell model. The levels of circ_DROSHA, myocyte-specific enhancer factor 2C (MEF2C) and miR-106b-5p were determined by qRT-PCR and western blot. Cell proliferation was detected by the Cell Counting-8 Kit (CCK-8) assay, and cell apoptosis was measured by flow cytometry. Targeted relationships among circ_DROSHA, miR-106b-5p and MEF2C were confirmed by a dual-luciferase reporter or RNA immunoprecipitation (RIP) assay. Our data showed that circ_DROSHA was down-regulated in the serum samples of TLE patients and the TLE cell model. Circ_DROSHA up-regulation alleviated the cytotoxicity of the TLE cell model by enhancing cell proliferation and repressing cell apoptosis. Circ_DROSHA directly bound to miR-106b-5p. Moreover, miR-106b-5p represented a downstream effector of circ_DROSHA function. MEF2C was a direct target of miR-106b-5p, and miR-106b-5p knockdown relieved magnesium-free treatment-induced cell injury by up-regulating MEF2C. Furthermore, circ_DROSHA regulated MEF2C expression via sponging miR-106b-5p. Our study suggested that the enforced expression of circ_DROSHA alleviated the cell damage of the TLE cell model at least in part through the regulation of the miR-106b-5p/MEF2C axis.

Integrated analysis of energy, indoor environment, and occupant satisfaction in green buildings using real-time monitoring data and on-site investigation.

Recently, a growing literature pay attention to the green buildings, and most of them focuses on design, energy simulation, and post-occupancy evaluation but rarely involves the integration analysis of energy consumption, indoor environmental quality, and occupant satisfaction in the operational stage. In this paper, the authors propose a comprehensive quantitative study based on energy-environment-satisfaction (EES) and take a three-star green building in Shanghai as an example. Through the use of real-time monitoring data, the study analyses the distribution characteristics of the parameters of EES. Meanwhile, this study discusses the differences between operational energy consumption and design parameters and also quantifies the exponential relationship between per floor personnel density and building energy consumption. Moreover, combined with the user satisfaction survey, some improvements are suggested. Furthermore, the relationship between daily energy consumption and the environmental parameters of daily energy consumption, PM2.5, CO2, temperature, relative humidity, and illumination is fitted, and the results indicate that there is a multivariate linear relationship with a correlation of 0.876. Through the sensitivity analysis, we found that the relative humidity affects 1.4 times as much as CO2. Therefore, its control value is critical to reduce energy consumption in the operation of green buildings.

Umbilical cord blood-based gene signatures related to prenatal major depressive disorder.

BACKGROUND: Prenatal exposure to depression has been considered as a risk factor for adverse childhood, while it is accompanied by unknown molecular mechanisms. The aim of this study was to identify differentially expressed genes (DEGs) and associated biological processes between cord blood samples from neonates born to mothers who exposed to major depressive disorder (MDD) and healthy mothers. METHODS: The microarray data GSE114852 were downloaded to analyze the mRNA expression profiles of umbilical cord blood with 31 samples exposed to prenatal MDD and 62 samples with healthy mothers. Kyoto Encyclopedia of Genes and Genomes pathway and Gene ontology enrichment analyses were conducted to identify associated biochemical pathways and functional categories of the DEGs. The protein-protein interaction network was constructed and the top 10 hub genes in the network were predicted. RESULTS: The results showed several immunity related processes, such as "phagosome", "Epstein-Barr virus infection", "proteasome", "positive regulation of I-kappaB kinase/NF-kappaB signaling", "interferon-gamma-mediated signaling pathway", and "tumor necrosis factor" presented significant differences between two groups. Most of the hub genes (for example PSMD2, PSMD6, PSMB8, PSMB9) were also associated with immune pathways. CONCLUSION: This bioinformatic analysis demonstrated immune-mediated mechanisms might play a fatal role in abnormalities in fetal gene expression profiles caused by prenatal MDD.

Long non-coding RNA CCAT1 promotes glioma cell proliferation via inhibiting microRNA-410.

BACKGROUND AND AIM: Long non-coding RNAs have been confirmed to play a critical role in various cancers. In the present study, the effect of long non-coding RNA (lncRNA) CCAT1 on glioma cell proliferation and its potential mechanism were investigated. METHODS AND RESULTS: Real-time PCR results showed that lncRNA-CCAT1 expression was significantly upregulated in glioma cancer tissues and cell lines compared with controls. After inhibiting CCAT1 expression in glioma cell line U251 with siRNA-CCAT1 (si-CCAT1), the cell viability and cell colony formation were decreased, the cell cycle was arrested in G1 phase, and the cell apoptosis was increased. As reported in bioinformatics software starbase2.0, a total of 22 microRNAs were potentially targeted by CCAT1. It was confirmed that miR-410 was altered most by si-CCAT1. After up-regulating CCAT1 expression in U251 cells, miR-410 level was decreased. Luciferase reporter assay confirmed that CCAT1 targeted miR-410. Correlation analysis showed that CCAT1 expression was negatively related to miR-410 expression in glioma cancer tissues. In addition, down-regulation of miR-410 reversed the inhibitory effect of si-CCAT1 on glioma proliferation. CONCLUSION: These data demonstrated that lncRNA-CCAT1 promoted glioma cell proliferation via inhibiting miR-410, providing a new insight about the pathogenesis of glioma proliferation.

Beta-asarone protects against MPTP-induced Parkinson's disease via regulating long non-coding RNA MALAT1 and inhibiting α-synuclein protein expression.

OBJECTIVE: Numerous long non-coding RNAs (lncRNA) have been identified in neurodegenerative disorders including Parkinson's disease (PD). Emerging evidence demonstrates that ß-asarone functions as neuroprotective effects in both in vitro and in vivo models. However, the role of ß-asarone and its potential mechanism in PD remain not completely clear. METHODS: MPTP-induced PD mouse model and SH-SY5Y cells subjected to MPP+ as its in vitro model were used to evaluate the effects of ß-asarone on PD. LncRNA MALAT1 and α-synuclein expression were determined by real-time PCR and western blot methods. RESULTS: ß-Asarone significantly increased the TH+ cells number and decreased the expression levels of MALAT1 and α-synuclein in midbrain tissue of PD mice. RNA pull-down and immunoprecipitation assays confirmed that MALAT1 associated with α-synuclein, leading to the increased stability of α-synuclein and its expression in SH-SY5Y cells. ß-asarone elevated the viability of cells exposed to MPP+. Either overexpressed MALAT1 or α-synuclein could canceled the protective effect of ß-asarone on cell viability. In PD mice, pcDNA-MALAT1 also decreased the TH+ cells number and increased the α-synuclein expression in PD mice with treatment of ß-asarone. CONCLUSION: ß-Asarone functions as a neuroprotective effect in both in vivo and in vitro models of PD via regulating MALAT1 and α-synuclein expression.

MicroRNA-214 participates in the neuroprotective effect of Resveratrol via inhibiting α-synuclein expression in MPTP-induced Parkinson's disease mouse.

BACKGROUNDS AND AIMS: MicroRNAs (miRNAs) have been reported to be involved in degenerative disorders including Parkinson's disease (PD). α-synuclein expression is strong associated with the pathogenesis of PD. In the present study, we investigated whether the regulation of α-synuclein expression by miR-214 is the potential mechanism underlying the neuroprotective effect of Resveratrol. METHODS: The PD mouse model was established with the injection of MPTP (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and the human neuroblastoma cell line, SH-SY5Y, was administrated with MPP+. RESULTS: The midbrain of PD mice and MPP+ treated SH-SY5Y cells had the lower expression levels of miR-214 and higher mRNA and protein expression of α-synuclein, which were reversed by Resveratrol administration. MiR-214 mimic down-regulated expression of α-synuclein and its 3'-UTR activity, while the levels were up-regulated by miR-214 inhibitor. In addition, the cell viability, elevated by Resveratrol, was also decreased by miR-214 inhibitor or overexpressed α-synuclein. In vivo, miR-214 inhibitor down-regulated TH+ cells of ipsilateral and up-regulated α-synuclein expression compared with the group treated with Resveratrol. CONCLUSION: The loss of miR-214 in PD resulted in the increase of α-synuclein expression, which was the potential mechanism underlying the neuroprotective effects of Resveratrol.

TGF-ß induced miR-132 enhances the activation of TGF-ß signaling through inhibiting SMAD7 expression in glioma cells.

Transforming growth factors ß (TGF-ß) pathway has been proven to play important roles in oncogenesis and angiogenesis of gliomas. MiR-132 might be related to TGF-ß signaling pathway and high miR-132 expression was reported to be a biomarker of poor prognosis in patients diagnosed with glioma. However, the expression regulation way involved in TGF-ß pathway and clinical significance of miR-132 have not been investigated in glioma cells. Here we reported that the mRNA level of miR-132 and TGF-ß concentration were both increased in patients with brain glioma. Correlation analysis revealed that TGF-ß concentration was positively correlated with mRNA level of miR-132. In addition, the mRNA level of miR-132 was up-regulated by TGF-ß in a concentration-dependent and time-dependent manner. Furthermore, we found that miR-132 was involved in modulation of the TGF-ß signaling pathway and down-regulation of SMAD7 expression by directly targeting the SMAD7 3'-UTR. MiR-132 was negatively correlated with SMAD7 in patients with brain glioma. Taken together, our results suggest that miR-132 could be stimulated by TGF-ß and might enhance the activation of TGF-ß signaling through inhibiting SMAD7 expression in glioma cells. These findings contribute to a better understanding of the mechanism of the activation of TGF-ß signaling by miR-132.