N-methyladenosine mediated-NRF2 signaling pathway attenuates cadmium cytotoxicity by inhibiting oxidative damage in bronchial epithelial cells.

Although N-methyladenosine (mA) and its regulatory proteins were involved in multiple cellular damage processes, the roles of mA and its regulatory proteins in cadmium-induced pulmonary cell damage remain largely unknown. Our present data indicated that cadmium exposure caused serious damage in bronchial epithelial cells, as evidenced by reduction of cell viability and elevation of oxidative damage and apoptosis. These processes were accompanied by alterations of mA modification and its regulatory proteins (FTO, ALKBH5, YTHDC2).

Emerging roles of N-methyladenosine in arsenic-induced toxicity.

Arsenic can cause extensive toxic damage after entering the body of humans and animals by altering a variety of events. As the most common form of methylation modification of RNA in eukaryotic cells, N-methyladenosine (mA) is widely involved in regulating RNA processing, translation and degradation, thus playing important role in various pathophysiological processes. Emerging studies have demonstrated that mA modification is synergistically mediated by methyltransferases, demethylases and methyl-binding proteins.

Screening of differentially expressed RNAs and identifying a ceRNA axis during cadmium-induced oxidative damage in pancreatic β cells.

Cadmium, a common metal pollutant, has been demonstrated to induce type 2 diabetes by disrupting pancreatic β cells function. In this study, transcriptome microarray was utilized to identify differential gene expression in oxidative damage to pancreatic β cells following cadmium exposure. The results indicated that a series of mRNAs, LncRNAs, and miRNAs were altered.

Roles of mA modification in regulating PPER pathway in cadmium-induced pancreatic β cell death.

Cadmium can lead to the death of pancreatic β cells, thus affecting the synthesis and secretion of insulin. However, the specific mechanisms underlying the cadmium-induced pancreatic β cell death have not been fully understood. In this study, roles of mA modification in regulating protein processing in endoplasmic reticulum (PPER) pathway in cadmium-induced pancreatic β cell death were explored.

Changes of mA Regulatory Proteins and Nrf2 Signaling Molecules in Liver Tissue of Type 2 Diabetes Mellitus Rats.

Both dysregulation of N-methyladenosine (mA) regulatory proteins and Nrf2 signaling molecules are involved in the process of injury to multiple tissues. However, changes of mA regulatory proteins and Nrf2 signaling molecules in liver tissue of T2DM remain unclear. In present study, changes of mA regulatory proteins (Mettl3, Mettl16, Fto, Alkbh5 and Ythdc2) and Nrf2 signaling molecules (Nrf2, Sod1, Ho-1, Gclc) were detected in the liver tissues of T2DM rats, which constructed by high fat-diet feeding and intraperitoneal injection of streptozotocin.

Changes of RNA mA/mC Modification Regulatory Molecules in Ferroptosis of T2DM Rat Pancreas.

N-methyladenine (mA) and 5-methylcytosine (mC) are two common forms of RNA methylation that play an important role in the epigenetics of type 2 diabetes mellitus (T2DM). One type of cell death, ferroptosis, has been implicated in islet β-cell damage in T2DM. Notably, RNA methylation, an upstream regulatory mechanism of mRNAs, can regulate the expression of ferroptosis signaling molecules, thereby affecting cell proliferation and death.

Changes of LncRNAs during the Process of Antioxidants Antagonize Cadmium-Induced Oxidative Damage in Islet β Cells.

Long non-coding RNAs (LncRNAs) play important regulatory roles in oxidative damage. Resveratrol, curcumin, and cyanidin are phytogenic antioxidants widely existing in nature and they have been proved to antagonize certain heavy metal-induced oxidative damage in cells. However, can they antagonize oxidative damage induced by cadmium in islet β cells? Are their mechanisms of antagonizing oxidative damage related to LncRNAs? In this study, we first detected the cell viability of each group by CCK8 assay.

Effects of food wastes based on different components on digestibility and energy recovery in hydrogen and methane co-production.

This study was conducted for four organic fractions (carbohydrates, proteins, cellulose, lipids) at an inoculum concentration of 30 % and a total solid (TS) of 8 % to investigate the effect of the main components of food waste on the performance of the two-stage anaerobic digestion. The results showed that the gas phase products were closely related to the composition of the substrate, with the carbohydrate and lipid groups showing the best hydrogen (154.91 ± 2.

Emerging roles of epigenetics in lead-induced neurotoxicity.

Lead is a common environmental heavy metal contaminant. Humans are highly susceptible to lead accumulation in the body, which causes nervous system damage and leads to a variety of nervous system diseases, such as Alzheimer's disease, Parkinson's disease, and autism spectrum disorder. Recent research has focused on the mechanisms of lead-induced neurotoxicity at multiple levels, including DNA methylation, histone modifications, and non-coding RNAs, which are involved in various lead-induced nervous system diseases.

Novel insights into mutual regulation between N-methyladenosine modification and LncRNAs in tumors.

N-methyladenosine (mA), one of the most common RNA methylation modifications, has emerged in recent years as a new layer of the regulatory mechanism controlling gene expression in eukaryotes. As a reversible epigenetic modification, mA not only occurs on mRNAs but also on Long non-coding RNAs (LncRNAs). As we all known, despite LncRNAs cannot encode proteins, they affect the expression of proteins by interacting with mRNAs or miRNAs, thus playing important roles in the occurrence and development of a variety of tumors.

Emerging Mutual Regulatory Roles between mA Modification and microRNAs.

N-metyladenosine (mA), one of the most common RNA methylation modifications in mammals, has attracted extensive attentions owing to its regulatory roles in a variety of physiological and pathological processes. As a reversible epigenetic modification on RNAs, mA is dynamically mediated by the functional interplay among the regulatory proteins of methyltransferases, demethylases and methyl-binding proteins. In recent years, it has become increasingly clear that mA modification is associated with the production and function of microRNAs (miRNAs).

Effects of different low temperature conditions on anaerobic digestion efficiency of pig manure and composition of archaea community.

To explore the effect of low temperature on the anaerobic digestion of pig manure, the anaerobic digestion experiment was carried out under the conditions of inoculum concentration of 30% and TS of 8%. Five low-temperature gradients of 4, 8, 12, 16 and 20 °C were set to study the activities of gas production, pH, solluted chemical oxygen demand (SCOD), volatile fatty acids (VFAs), coenzymes F and archaea community composition in the digestion process. The results were demonstrated: as the temperature decreased, the more unstable the gas production became, the less gas production produced, and the later the gas peak occurred.

The association of high-fluoride and high-iodine combined exposure with dental fluorosis and goiter: a meta-analysis.

It is controversial that high-fluoride and high-iodine combined exposure affects the prevalence of dental fluorosis and goiter. The aim of this study was to explore the potential association between high-fluoride and high-iodine combined exposure with dental fluorosis and goiter. We retrieved relevant articles from PubMed, Cochrane Library, China National Knowledge Infrastructure, Wanfang Database and China Science and Technology Journal Database (VIP).

Study on the Correlation Between Regulatory Proteins of N-methyladenosine and Oxidative Damage in Cadmium-induced Renal Injury.

As a common environmental heavy metal pollutant, cadmium has been well evidenced to cause kidney damage; yet, the underlying mechanisms are still not fully clarified. In this study, cell viability of human renal tubular epithelial cell (HK-2) was determined by CCK-8 assay after treatment with CdSO. Then, apoptotic morphology of cells was observed by Hoechst staining and level of reactive oxygen species (ROS) was detected by fluorescent probes.

Controlled Release of Insulin Based on Temperature and Glucose Dual Responsive Biomicrocapsules.

The treatment of diabetes lies in developing novel functional carriers, which are expected to have the unique capability of monitoring blood glucose levels continuously and dispensing insulin correctly and timely. Hence, this study is proposing to create a smart self-regulated insulin delivery system according to changes in glucose concentration. Temperature and glucose dual responsive copolymer microcapsules bearing -isopropylacrylamide and 3-acrylamidophenylboronic acid as main components were developed by bottom-spray coating technology and template method.

The effect of anaerobic co-fermentation on acidification performance of food waste and cardboard waste.

The fermentation system with high solid materials for food waste (FW) is uneven in nutrition and easy to produce volatile acid accumulation, which causes the reaction system to acidify and affects the normal operation of fermentation. This study evaluated the effect of the co-substrate percentages (FW:CB = 9:1, FW:CB = 8:2, FW:CB = 7:3) and the initial total solid contents (12%, 15%, 18%) on the co-fermentation acidification performance of FW and cardboard waste (CB). The maximum methane production was obtained when mono-fermenting FW had high solids contents (1.

Changes and relationship of N-methyladenosine modification and long non-coding RNAs in oxidative damage induced by cadmium in pancreatic β-cells.

N-methyladenosine (mA) modification and mA-modified Long non-coding RNAs (LncRNAs) play crucial roles in various pathological processes, yet their changes and relationship in cadmium-induced oxidative damage are largely unknown. Here, five mA-modified LncRNAs (LncRNA-TUG1, LncRNA-PVT1, LncRNA-MALAT1, LncRNA-XIST, LncRNA-NEAT1), which have been evidenced to involve in oxidative damage, were selected and their binding proteins were submitted to bioinformatics analysis. Our analysis results showed that these five mA-modified LncRNAs bound to different regulatory proteins of mA modification, implicating that mA modification on LncRNAs may synergistically control by multiple regulatory proteins.

[Inhibition of WIP1 in A549 cells enhances the sensitivity of cells to arsenic treatment].

Objective: To explore if inhibiting the expression of wild-type p53-induced phosphatase 1( WIP1) could enhance the sensitivity of A549 cells to arsenic.

Methods: To inhibit expression of WIP1, WIP1 siRNA was transferred into A549 cells by using Lipofectamine 2000. Then the protein expression levels of P53 phosphorylation proteins and their downstream effectors were detected by western-blot analysis.

N-methyladenosine mediates the cellular proliferation and apoptosis via microRNAs in arsenite-transformed cells.

N-methyladenosine (mA) modification is implicated to play an important role in cellular biological processes, but its regulatory mechanisms in arsenite-induced carcinogenesis are largely unknown. Here, human bronchial epithelial (HBE) cells were chronically treated with 2.5 μM arsenite sodium (NaAsO) for about 13 weeks and these cells were identified with malignant phenotype which was demonstrated by increased levels of cellular proliferation, percentages of plate colony formation and soft agar clone formation, and high potential of resistance to apoptotic induction.

Regulation of ABCG2 by nuclear factor kappa B affects the sensitivity of human lung adenocarcinoma A549 cells to arsenic trioxide.

Arsenic trioxide (AsO) is successfully used as an anticancer agent against acute promyelocytic leukemia and some solid tumors. However, the application of AsO is largely limited by its drug resistance in the treatment of non-small cell lung carcinoma (NSCLC). Therefore, it is an urgent task to enhance the sensitivity of lung cancer cells to AsO.

[miR-155/BACH1 Signaling Pathway in Human Lung Adenocarcinoma Cell Death Induced by Arsenic Trioxide].

Objective: To explore the changes of micro RNA 155 (miR-155),BTB and CNC homologous protein 1 (BACH1),quinone oxidoreductase 1 (NQO1) and heme-oxygenase-1 (HO-1) in the process of arsenic trioxide-induced cell death,and to clarify the relationship between miR-155 and BACH1,providing experimental basis for the sensitivity of arsenic trioxide (ATO) treatment.

Methods: Human lung adenocarcinoma cell line A549 cells were treated with different concentrations of ATO. MTT assay and total antioxidant capacity detection kit were used to determine cell viability and total antioxidant capacity,respectively.

The selectivity of artemisinin-based drugs on human lung normal and cancer cells.

Artemisinin-based drugs are documented to possess anticancer potential that is selectively effective to cancer cells. However, this selectivity is disputable in different studies and the mechanism is still unclear. To clarify this discrepancy, this study employed five assays to evaluate the cytotoxic effects of artemisinin and artesunate on normal human bronchial epithelial (HBE) cells and lung adenocarcinoma A549 cells.

Alterations of miRNAs and Their Potential Roles in Arsenite-Induced Transformation of Human Bronchial Epithelial Cells.

The alterations of micro RNAs (miRNAs) and their potential roles in arsenite-induced tumorigenesis are still poorly understood. In this study, miRNA Array was used to detect the expression level of miRNAs in human bronchial epithelial (HBE) cells that were transformed by 2.5 μM arsenite for 13 weeks.

miR-155 mediates arsenic trioxide resistance by activating Nrf2 and suppressing apoptosis in lung cancer cells.

Arsenic trioxide (ATO) resistance is a challenging problem in chemotherapy. However, the underlying mechanisms remain to be elucidated. In this study, we identified a high level of expression of miR-155 in a human lung adenocarcinoma A549R cell line that is highly resistant to ATO.