Enhanced photoconduction of free-standing ZnO nanowire films by L-lysine treatment

Flexible paper-like ZnO nanowire films are fabricated and the effect of L-lysine passivation of the nanowire surfaces on improving the UV photoresponse is studied. We prepare three types of nanowires with different defect contents, and find that the L-lysine treatment can suppress the oxygen-vacancy-related photoluminescence as well as enhance the UV photoconduction. The nanowires with fewer defects gain larger enhancement of UV photoconduction after L-lysine treatment. Reproducible UV photoresponse of the devices in humid air is obtained due to L-lysine surface passivation, ruling out the influence of water molecules in degrading the UV photocurrent

Identification of senescence-associated genes in human bone marrow mesenchymal stem cells

Human bone marrow mesenchymal stem cells (hBMMSCs) are multipotent stem cells that can differentiate into several specialized cell types, including bone, cartilage, and fat cells. The proliferative capacity of hBMMSCs paves the way for the development of regenerative medicine and tissue engineering. However, long-term in vitro culture of hBMMSCs leads to a reduced life span of the cells due to senescence, which leads eventually to growth arrest. To investigate the molecular mechanism behind the cellular senescence of hBMMSCs, microarray analysis was used to compare the expression profiles of early passage hBMMSCs, late passage hBMMSCs and hBMMSCs ectopically expressing human telomerase reverse transcriptase (hTERT). Using an intersection analysis of 3892 differentially expressed genes (DEGs) out of 27,171 total genes analyzed, we identified 338 senescence-related DEGs. GO term categorization and pathway network analysis revealed that the identified genes are strongly related to known senescence pathways and mechanisms. The genes identified using this approach will facilitate future studies of the mechanisms underlying the cellular senescence of hBMMSCs

8-OxoG in GC-rich Sp1 binding sites enhances gene transcription in adipose tissue of juvenile mice

The oxidation of guanine to 8-oxoguanine (8-oxoG) is the most common type of oxidative DNA lesion. There is a growing body of evidence indicating that 8-oxoG is not only pre-mutagenic, but also plays an essential role in modulating gene expression along with its cognate repair proteins. In this study, we investigated the relationship between 8-oxoG formed under intrinsic oxidative stress conditions and gene expression in adipose and lung tissues of juvenile mice. We observed that transcriptional activity and the number of active genes were significantly correlated with the distribution of 8-oxoG in gene promoter regions, as determined by reverse-phase liquid chromatography/mass spectrometry (RP-LC/MS), and 8-oxoG and RNA sequencing. Gene regulation by 8-oxoG was not associated with the degree of 8-oxoG formation. Instead, genes with GC-rich transcription factor binding sites in their promoters became more active with increasing 8-oxoG abundance as also demonstrated by specificity protein 1 (Sp1)- and estrogen response element (ERE)-luciferase assays in human embryonic kidney (HEK293T) cells. These results indicate that the occurrence of 8-oxoG in GC-rich Sp1 binding sites is important for gene regulation during adipose tissue development.Y

LncRNA LINC00240 suppresses invasion and migration in non-small cell lung cancer by sponging miR-7-5p

Background lncRNAs have important roles in regulating cancer biology. Accumulating evidence has established a link between the dysregulation of lncRNAs and microRNA in cancer progression. In previous studies, miR-7-5p has been found to be significantly down-regulated in mesenchymal-like lung cancer cell lines and directly regulated EGFR. In this work, we investigated the lncRNA partner of miR-7-5p in the progression of lung cancer. Methods We investigated the expression of miR-7-5p and the lncRNA after transfection with an miR-7-5p mimics using a microarray. The microarray results were validated using quantitative real time-polymerase Chain Reaction (qRT-PCR). The regulatory effects of lncRNA on miR-7-5p and its target were evaluated by changes in the expression of miR-7-5p after transfection with siRNAs for lncRNA and the synthesis of full-length lncRNA. The effect of miR-7-5p on lncRNA and the miRNA target was evaluated after transfection with miRNA mimic and inhibitor. The role of lncRNA in cancer progression was determined using invasion and migration assays. The level of lncRNA and EGFR in lung cancer and normal lung tissue was analyzed using TCGA data. Results We found that LINC00240 was downregulated in lung cancer cell line after miR-7-5p transfection with an miR-7-5p mimic. Further investigations revealed that the knockdown of LINC00240 induced the overexpression of miR-7-5p. The overexpression of miR-7-5p diminished cancer invasion and migration. The EGFR expression was down regulated after siRNA treatment for LINC00240. Silencing LINC00240 suppressed the invasion and migration of lung cancer cells, whereas LINC00240 overexpression exerted the opposite effect. The lower expression of LINC00240 in squamous lung cancer was analyzed using TCGA data. Conclusions Taken together, LINC00240 acted as a sponge for miR-7-5p and induced the overexpression of EGFR. LINC00240 may represent a potential target for the treatment of lung cancer.All of this study was supported by a National Research Foundation of Korea Grant funded by the Korean Government (NRF-2018R1D1A3B07048311 and NRF-2018R1D1A3B07045878)

Differential expression levels of 8-oxoG repair genes <i>Ogg1</i> and <i>PolB</i> in ESCs induced by oxidative stress.

<p>Relative mRNA levels of (A) <i>Ogg1</i> mRNA and (B) <i>PolB</i>. Gapdh was used as an internal control. Mean ± SD, **<i>p</i> < 0.01, ***<i>p</i> < 0.001, one-sided t-test. (C) Levels of Ogg1 and PolB proteins by Western blotting. α-tubulin was used as an internal control.</p

Sequences surrounding the transcription start sites of <i>Mef2C</i>, <i>Nkx2-5</i>, and <i>Gata4</i> genes in R1 mouse ESCs subjected to oxidative stress.

<p>Sequences surrounding the transcription start sites of <i>Mef2C</i>, <i>Nkx2-5</i>, and <i>Gata4</i> genes in R1 mouse ESCs subjected to oxidative stress.</p

Effects of oxidative stress on R1 mouse ESC proliferation and differentiation.

<p>(A) Proliferation of ESCs after oxidative stress induced for two days by removing 2-mercaptoethanol (2ME) from ESC medium. *<i>p</i> < 0.05, Welch t-test. Means of fold changes with standard errors were presented. (B) Different EB morphologies from (+)2ME and (-)2ME media (bar = 100 μm) and (C) the percentages of beating EBs were observed from oxidative-stressed ESCs vs. controls (**<i>p</i> < 0.01, one-sided t-test).</p

G∙C to C∙G transversions at exon 1 of the <i>Tbx5</i> gene in R1 mouse ESCs subjected to oxidative stress.

<p>G∙C to C∙G transversions at exon 1 of the <i>Tbx5</i> gene in R1 mouse ESCs subjected to oxidative stress.</p

Establishment of the Hoogsteen base pairing-mediated PCR-Sequencing assay for 8-oxoG lesions in DNA.

<p>(A) pUC19oxoG(+) was prepared by site-directed mutagenesis, (B) 8-oxoG lesion was identified by Hind III resistance, and (C) Hoogsteen base pairing-mediated 8-oxoG to T transversion. T4: T4 DNA ligase, HIII: Hind III restriction enzyme.</p