INTRODUCTION: Long noncoding RNA PMS2L2 can inhibit inflammation induced by LPS, while LPS plays an important role in sepsis, indicating the possible involvement of PMS2L2 in sepsis. METHODS: Expressions of miR-21 and PMS2L2 in patients with acute kidney injury (AKI), sepsis patients without induced AKI, and healthy controls were determined by performing RT-qPCR. Overexpression assay was performed to explore the crosstalk between miR-21 and PMS2L2. Methylation-specific PCR (MSP) was performed to explore the role of PMS2L2 in regulating the methylation of miR-21 gene. The role of miR-21 and PMS2L2 in the apoptosis of CIHP-1 cells induced by LPS was assessed by cell apoptosis assay. RESULTS: PMS2L2 was downregulated in AKI patients induced by sepsis compared to sepsis patients without AKI and healthy controls. MiR-21 was also downregulated in AKI induced by sepsis and positively correlated with PMS2L2. In addition, in cells of human podocyte cell line (CIHP-1), overexpression of PMS2L2 promoted the expression of miR-21, while miR-21 did not affect the expression of PMS2L2. MSP analysis showed that overexpression of PMS2L2 decreased methylation of miR-21. LPS treatment downregulated PMS2L2 and miR-21 in a time-dependent manner. PMS2L2 and miR-21 decreased the apoptosis of CIHP-1 cells induced by LPS, and co-overexpression of PMS2L2 and miR-21 showed stronger inhibitory effect. CONCLUSION: PMS2L2 is downregulated in AKI induced by sepsis and inhibits LPS-induced apoptosis of podocytes.
Acute Kidney Injury , MicroRNAs , Podocytes , RNA, Long Noncoding , Sepsis , Humans , Podocytes/metabolism , MicroRNAs/genetics , MicroRNAs/metabolism , RNA, Long Noncoding/genetics , Lipopolysaccharides/pharmacology , Acute Kidney Injury/genetics , Acute Kidney Injury/metabolism , Apoptosis , Sepsis/complications
Exploration of new superconductors has always been one of the research directions in condensed matter physics. We report here a new layered heterostructure of [(Fe,Al)(OH)2][FeSe]1.2, which is synthesized by the hydrothermal ion-exchange technique. The structure is suggested by a combination of X-ray powder diffraction and the electron diffraction (ED). [(Fe,Al)(OH)2][FeSe]1.2 is composed of the alternating stacking of a tetragonal FeSe layer and a hexagonal (Fe,Al)(OH)2 layer. In [(Fe,Al)(OH)2][FeSe]1.2, there exists a mismatch between the FeSe sublayer and the (Fe,Al)(OH)2 sublayer, and the lattice of the layered heterostructure is quasi-commensurate. The as-synthesized [(Fe,Al)(OH)2][FeSe]1.2 is nonsuperconducting due to the Fe vacancies in the FeSe layer. The superconductivity with a Tc of 40 K can be achieved after a lithiation process, which is due to the elimination of the Fe vacancies in the FeSe layer. The Tc is nearly the same as that of (Li,Fe)OHFeSe although the structure of [(Fe,Al)(OH)2][FeSe]1.2 is quite different from that of (Li,Fe)OHFeSe. The new layered heterostructure of [(Fe,Al)(OH)2][FeSe]1.2 contains an iron selenium tetragonal lattice interleaved with a hexagonal metal hydroxide lattice. These results indicate that the superconductivity is very robust for FeSe-based superconductors. It opens a path for exploring superconductivity in iron-base superconductors.
Various liver diseases caused by liver damage seriously affect people's health. The purpose of this study was to clarify the effects and the mechanisms of carnitine palmitoyltransferase 1 (Cpt1a) on oxidative stress and inflammation in liver injury. It was found that the expression of Cpt1a mRNA was upregulated in a model of liver injury in mice. Thus, overexpression of Cpt1a increased reactive oxygen species (ROS) production and malondialdehyde (MDA) levels and reduced superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-px) levels in an in vitro model of liver injury. It was also shown that overexpression of Cpt1a suppressed the nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In summary, these data indicate that Cpt1a promotes ROS-induced oxidative stress in liver injury via the Nrf2/HO-1 and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome signaling pathway.
Heme Oxygenase-1 , Animals , Inflammasomes/metabolism , Male , Mice , NF-E2-Related Factor 2/metabolism , Reactive Oxygen Species/metabolism
BACKGROUND: Breast cancer (BC) is a huge health threat for women worldwide. Although numerous microRNAs (miRNA) have been found to be aberrantly expressed in BC, the construction of a comprehensive miRNA-messenger RNA (mRNA) network is still needed. METHODS: Limma package was used to identify differentially expressed miRNAs (DEMs) in microarray datasets downloaded from GEO database. Genes targeted by DEMs were analyzed using mirTarBase. Gene Ontology and pathway enrichment analysis for these genes were performed at DAVID. Expression correlations of DEMs and target genes were analyzed at ENCORI. Based on these results, a miRNA-mRNA regulatory network was constructed. RESULTS: A total of 17 overlapping DEMs were identified at these two microarray datasets. Expression of DEMs in BC tissues compared with normal tissues were further validated by ENCORI. By utilizing miRTarBase, a total of 167 target genes for DEMs were obtained. 10 hub genes (AKT1, MYC, VEGFA, CCND1, PTEN, IL6, CASP3, KRAS, IGF1, ESR1) were identified. Through analyzing the effects of hub genes on overall survival of BC patients and their expression correlation with miRNAs, we found hsa-miR-98-5p/IGF1 axis may play a crucial role in BC progression. The connections of hsa-miR-98-5p and IGF1 were further validated by luciferase activity reporter assay and functional assays. CONCLUSIONS: In this work, a miRNA-mRNA network related to BC progression was built, and identified one important miRNA-mRNA axis in BC.
Breast Neoplasms/genetics , Gene Expression Regulation, Neoplastic , Gene Regulatory Networks , Insulin-Like Growth Factor I/genetics , MicroRNAs/genetics , Animals , Cell Line, Tumor , Computational Biology , Disease Progression , Female , Gene Ontology , Humans , Mice, Inbred BALB C , Mice, Nude
The long noncoding RNA component of mitochondrial RNA-processing endoribonuclease (lncRNA RMRP) plays an important role in tumor development. In the present study, we determined the regulatory function of RMRP in non-small-cell lung cancer (NSCLC). The NSCLC tissues and the adjacent nontumor tissues were collected for the study. The RMRP expression was detected by quantitative real time-PCR in NSCLC and lung cancer cell lines. The functional validation experiments were performed to determine the role of RMRP on NSCLC progression. In addition, we identified the downstream target miRNAs for RMRP. The results showed that RMRP was elevated in NSCLC tissues and cell lines. High RMRP expression was closely associated with advanced stage for the clinical features and low overall survival in NSCLC patients. Functional assay showed that loss of RMRP markedly inhibited cell proliferation, migration, and invasion. Flow cytometry assay demonstrated that the inhibition of RMRP dramatically induced cell cycle arrest in the G0/G1 phase. Moreover, we found that the role of RMRP on NSCLC cell progression was modulated by the inhibition of miR-1-3p. Collectively, our results demonstrated that the "RMRP-miR-1-3p" axis might promote NSCLC progression. Hence, these investigations will provide a therapeutic target and strategy for the treatment of NSCLC progression.
Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/pathology , Lung Neoplasms/genetics , Lung Neoplasms/pathology , MicroRNAs/metabolism , RNA, Long Noncoding/metabolism , Annexin A2/genetics , Annexin A2/metabolism , Base Sequence , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Female , Gene Expression Regulation, Neoplastic , Gene Knockdown Techniques , History, 17th Century , Humans , Male , MicroRNAs/genetics , Neoplasm Invasiveness , RNA, Long Noncoding/genetics , Up-Regulation/genetics
Thermoelectric materials can be used to convert heat to electric power through the Seebeck effect. We study magneto-thermoelectric figure of merit (ZT) in three-dimensional Dirac semimetal Cd3As2 crystal. It is found that enhancement of power factor and reduction of thermal conductivity can be realized at the same time through magnetic field although magnetoresistivity is greatly increased. ZT can be highly enhanced from 0.17 to 1.1 by more than six times around 350â¯K under a perpendicular magnetic field of 7â¯T. The huge enhancement of ZT by magnetic field arises from the linear Dirac band with large Fermi velocity and the large electric thermal conductivity in Cd3As2. Our work paves a new way to greatly enhance the thermoelectric performance in the quantum topological materials.
