Carbon black nanoparticles and cadmium co-exposure aggravates bronchial epithelial cells inflammation via autophagy-lysosome pathway.

Carbon black nanoparticles (CBNPs) and cadmium (Cd) are major components of various air pollutants and cigarette smoke. Autophagy and inflammation both play critical roles in understanding the toxicity of particles and their components, as well as maintaining body homeostasis. However, the effects and mechanisms of CBNPs and Cd (CBNPs-Cd) co-exposure on the human respiratory system remain unclear. In this study, a CBNPs-Cd exposure model was constructed to explore the respiratory toxicity and combined mechanism of these chemicals on the autophagy-lysosome pathway in the context of respiratory inflammation. Co-exposure of CBNPs and Cd significantly increased the number of autophagosomes and lysosomes in human bronchial epithelial cells (16HBE) and mouse lung tissues compared to the control group, as well as the groups exposed to CBNPs and Cd alone. Autophagic markers, LC3II and P62 proteins, were up-regulated in 16HBE cells and mouse lung tissues after CBNPs-Cd co-exposure. However, treatment with Cq inhibitor (an indicator of lysosomal acid environment) resulted in a substantial decreased co-localization fluorescence of LC3 and lysosomes in the CBNPs-Cd combination group compared with the CBNPs-Cd single and control groups. No difference in LAMP1 protein expression was observed among the exposed groups. Adding 3 MA alleviated inflammatory responses, while applying the Baf-A1 inhibitor aggravated inflammation both in vitro and in vivo following CBNPs-Cd co-exposure. Factorial analysis showed no interaction between CBNPs and Cd in their effects on 16HBE cells. We demonstrated that co-exposure to CBNPs-Cd increases the synthesis of autophagosomes and regulates the acidic environment of lysosomes, thereby inhibiting autophagy-lysosome fusion and enhancing the inflammatory response in both 16HBE cells and mouse lung. These findings provide evidence for a comprehensive understanding of the interaction between CBNPs and Cd in mixed pollutants, as well as for the prevention and control of occupational exposure to these two chemicals.

Microplastics alter the equilibrium of plant-soil-microbial system: A meta-analysis.

Microplastics (MPs) are widely identified as emerging hazards causing considerable eco-toxicity in terrestrial ecosystems, but the impacts differ in different ecosystem functions among different chemical compositions, morphology, sizes, concentrations, and experiment duration. Given the close relationships and trade-offs between plant and soil systems, probing the "whole ecosystem" instead of individual functions must yield novel insights into MPs affecting terrestrial ecosystems. Here, a comprehensive meta-analysis was employed to reveal an unambiguous response of the plant-soil-microbial system to MPs. Results showed that in view of plant, soil, and microbial functions, the general response patterns of plant and soil functions to MPs were obviously opposite. For example, polyethylene (PE) and polyvinyl chloride (PVC) MPs highly increased plant functions, while posed negative effects on soil functions. Polystyrene (PS) and biodegradable (Bio) MPs decreased plant functions, while stimulating soil functions. Additionally, low-density polyethylene (LDPE), PE, PS, PVC, Bio, and granular MPs significantly decreased soil microbial functions. These results clearly revealed that MPs alter the equilibrium of the plant-soil-microbial system. More importantly, our results further revealed that MPs tended to increase ecosystem multifunctionality, e.g., LDPE and PVC MPs posed positive effects on ecosystem multifunctionality, PE, PS, and Bio MPs showed neutral effects on ecosystem multifunctionality. Linear regression analysis showed that under low MPs size (<100 µm), ecosystem multifunctionality was gradually reduced with the increased size of MPs. The response of ecosystem multifunctionality showed a concave shape pattern along the gradient of experimental duration which was lower than 70 days. More importantly, there was a threshold (i.e., 5% w/w) for the effects of MPs concentration on ecosystem multifunctionality, i.e., under low concentration (< 5% w/w), ecosystem multifunctionality was gradually increased with the increased concentration of MPs, while ecosystem multifunctionality was gradually decreased under high concentration (i.e., > 5% w/w). These findings emphasize the importance of studying the effects of MPs on plant-soil-microbial systems and help us identify ways to reduce the eco-toxicity of MPs and maintain environmental safety in view of an ecology perspective.

Neglected Drivers of Antibiotic Resistance: Survival of Extended-Spectrum ß-Lactamase-Producing Pathogenic Escherichia coli from Livestock Waste through Dormancy and Release of Transformable Extracellular Antibiotic Resistance Genes under Heat Treatment.

Extended-spectrum ß-lactamase (ESBL)-producing Enterobacteriaceae has caused a global pandemic with high prevalence in livestock and poultry, which could disseminate into the environment and humans. To curb this risk, heat-based harmless treatment of livestock waste was carried out. However, some risks of the bacterial persistence have not been thoroughly assessed. This study demonstrated that antibiotic-resistant bacteria (ARB) could survive at 55 °C through dormancy, and simultaneously transformable extracellular antibiotic resistance genes (eARGs) would be released. The ESBL-producing pathogenic Escherichia coli CM1 from chicken manure could enter a dormant state at 55 °C and reactivate at 37 °C. Dormant CM1 had stronger ß-lactam resistance, which was associated with high expression of ß-lactamase genes and low expression of outer membrane porin genes. Resuscitated CM1 maintained its virulence expression and multidrug resistance and even had stronger cephalosporin resistance, which might be due to the ultra-low expression of the porin genes. Besides, heat at 55 °C promoted the release of eARGs, some of which possessed a certain nuclease stability and heat persistence, and even maintained their transformability to an Acinetobacter baylyi strain. Therefore, dormant multidrug-resistant pathogens from livestock waste will still pose a direct health risk to humans, while the resuscitation of dormant ARB and the transformation of released eARGs will jointly promote the proliferation of ARGs and the spread of antibiotic resistance.

Rice OsANN9 Enhances Drought Tolerance through Modulating ROS Scavenging Systems.

Drought is a critical abiotic stress which leads to crop yield and a decrease in quality. Annexins belong to a multi-gene family of calcium- and lipid-binding proteins and play diverse roles in plant growth and development. Herein, we report a rice annexin protein, OsANN9, which in addition to regular annexin repeats and type-II Ca2+ binding sites, also consists of a C2H2-type zinc-finger domain. We found that the expression of OsANN9 was upregulated by polyethylene glycol (PEG) or water-deficient treatment. Moreover, plants that overexpressed OsANN9 had increased survival rates under drought stress, while both OsANN9-RNAi and osann9 mutants showed sensitivity to drought. In addition, the overexpression of OsANN9 increased superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT) activities, which regulate reactive oxygen species homeostasis. Collectively, these findings indicate that OsANN9 may function as a positive regulator in response to drought stress by modulating antioxidant accumulation. Interestingly, the setting rates of osann9 mutant rice plants significantly decreased in comparison to wild-type plants, suggesting that OsANN9 might be involved in other molecular mechanisms in the rice seed development stage.

Phenotype and metabolism alterations in PCB-degrading Rhodococcus biphenylivorans TG9T under acid stress.

Environmental acidification impairs microorganism diversity and their functions on substance transformation. Rhodococcus is a ubiquitously distributed genus for contaminant detoxification in the environment, and it can also adapt a certain range of pH. This work interpreted the acid responses from both phenotype and metabolism in strain Rhodococcus biphenylivorans TG9T (TG9) induced at pH 3. The phenotype alterations were described with the number of culturable and viable cells, intracellular ATP concentrations, cell shape and entocyte, degradation efficiency of polychlorinated biphenyl (PCB) 31 and biphenyl. The number of culturable cells maintained rather stable within the first 10 days, even though the other phenotypes had noticeable alterations, indicating that TG9 possesses certain capacities to survive under acid stress. The metabolism responses were interpreted based on transcription analyses with four treatments including log phase (LP), acid-induced (PER), early recovery after removing acid (RE) and later recovery (REL). With the overview on the expression regulations among the 4 treatments, the RE sample presented more upregulated and less downregulated genes, suggesting that its metabolism was somehow more active after recovering from acid stress. In addition, the response mechanism was interpreted on 10 individual metabolism pathways mainly covering protein modification, antioxidation, antipermeability, H+ consumption, neutralization and extrusion. Furthermore, the transcription variations were verified with RT-qPCR on 8 genes with 24-hr, 48-hr and 72-hr acid treatment. Taken together, TG9 possesses comprehensive metabolism strategies defending against acid stress. Consequently, a model was built to provide an integrate insight to understand the acid resistance/tolerance metabolisms in microorganisms.

Circular RNA circSATB2 promotes progression of non-small cell lung cancer cells.

BACKGROUND: Lung cancer has high morbidity and mortality worldwide with non-small cell lung cancer (NSCLC) accounting for 85% of the cases. Therapies for lung cancer have relatively poor outcomes and further improvements are required. Circular RNAs have been reported to participate in the occurrence and progression of cancer. Information on the functions and mechanism of circRNAs in lung cancer is limited and needs more exploration. METHODS: We detected expression of genes and proteins by qPCR and western blot. Function of circSATB2 was investigated using RNA interference and overexpression assays. Location of circSATB2 was assessed by fluorescence in situ hybridization (FISH). Interaction of circSATB2, miR-326 and FSCN1 was confirmed by dual-luciferase reporter assay. RESULTS: Data from the investigation showed that circSATB2 was highly expressed in NSCLC cells and tissues. circSATB2 positively regulated fascin homolog 1, actin-bundling protein 1 (FSCN1) expression via miR-326 in lung cancer cells. Furthermore, circSATB2 can be transferred by exosomes and promote the proliferation, migration and invasion of NSCLC cells, as well as induce abnormal proliferation in normal human bronchial epithelial cells. Also, circSATB2 was highly expressed in serumal exosomes from lung cancer patients with high sensitivity and specificity for clinical detection and was related to lung cancer metastasis. CONCLUSIONS: circSATB2 participated in the progression of NSCLC and was differentially expressed in lung cancer tissue and serumal exosomes. circSATB2 may be potential biomarker for the diagnosis of NSCLC.

Mulberry anthocyanins exert anti-AGEs effects by selectively trapping glyoxal and structural-dependently blocking the lysyl residues of ß-lactoglobulins.

Advanced glycation end-products (AGEs), which instigate many disorders, are mostly mediated by dicarbonyl rearrangements. We studied the corresponding mechanisms of the anti-glycation effects of two anthocyanins purified from mulberry fruits, namely cyanidin 3-glucoside (C3G) and cyanidin 3-rutinoside (C3R), on glycated ß-lactoglobulins (ß-Lg). Both mulberry anthocyanins (MAs) inhibited the AGEs-formation in a dose-dependent manner, but the effect of C3R was significantly stronger than that of C3G (p < 0.05). MAs inhibited AGEs-formation by selectively trapping dicarbonyls, especially glyoxal. The UPLC-ESI-Q-TOF-MS results characterized that C3R formed mono- and di-glyoxal adducts, where C3G only created di-glyoxal adducts. Additionally, C3R could directly interact with some of the glycation sites of ß-Lg. Overall, GO-trapping and ß-Lg-MAs covalent/noncovalent binding are disclosed as the key mechanisms of the anti-AGEs activity of MAs on ß-Lg, which could be valorised as effectual AGEs inhibitors in proteins-rich matrices.

Simultaneous determination of the pharmacokinetics of A-type EGCG and ECG dimers in mice plasma and its metabolites by UPLC-QTOF-MS.

A-type epigallocatechin-3-gallate (EGCG) and epicatechin-3-O-gallate (ECG) dimers have multiply biological activities. In this study, the pharmacokinetics of them were investigated in mice after a single dose intravenous administration, and the metabolites in mice plasma and urine were investigated by ultra-performance liquid chromatography-Quadrupole-time of flight mass spectrometer (UPLC-QTOF-MS). Our results showed that the half-life (t1/2) of A-type EGCG and ECG dimers were 116.37 min and 33.04 min, respectively, and the maximal concentration in plasma was 32.81 µg/mL and 55.59 µg/mL, respectively. It was found that two dimers were firstly experienced by quinone methide (QM) fission to form the EGCG and ECG analogue, and the phase II metabolites were generated subsequently. The main metabolites in plasma and urine were glucuronidation and sulphation derivatives. In addition, small molecule weight of phenolic acids were detected in urine.

Transcription factor Tbx5 promotes cardiomyogenic differentiation of cardiac fibroblasts treated with 5-azacytidine.

Conversion of cardiac fibroblasts (CFs) into induced cardiomyocytes has recently been demonstrated, represents a potential therapeutic strategy for cardiac repair after myocardial injury. However, current approaches are inefficient. Here, we report that a defined transcription factor Tbx5, promoted cardiac reprogramming in the presence of a chemical inducer 5-azacytidine (5-aza). Morphological changes and cardiac specific genes and proteins expression were determined by immunofluorescence, quantitative real-time polymerase chain reaction, and Western blot analysis. Remarkably, Tbx5 enabled cardiac reprogramming with 5-aza by activating the expression of myocardial transcription-related genes, including cTnT, α-actin, Mef2c and inhibiting the expression of pluripotent genes such as Nanog, Oct4, and Sox2. Moreover, overexpression of Tbx5 upregulated the expression of sarcomere protein cTnT in CFs more efficiently at week 3 compared with 5aza-treated alone (P < 0.05). Conversely, inhibition of Tbx5 attenuated cardiac reprogramming. Furthermore, downregulated Tbx5 decreased wnt3a expression. At the same time, the inhibition effect of Tbx5i on cardiac reprogramming was reversed in vitro when these cells were exposed to Chir99021, a GSK-3 inhibitor. This finding provides new insight into the mechanism of cardiac reprogramming underlying the cardiac reprogramming process and lays the foundation for future clinical applications.

A new structure from cardiac cells cultured in vitro: Cardiomyocyte-annulation of neonatal rats.

To explore the formation, morphological characteristics, cell composition, and differentiation potential of cardiomyocyte annulation (cardio-annulation) during in vitro culture of cardiac cells. Cardiac cells were isolated and cultured. A live-cell imaging system was used to observe cardio-annulation. Cardiac troponin-T (cTnT) and vimentin were labeled with double immunofluorescence staining, and coexpressions of cTnT and connexin43 (Cx43), cTnT and nanog, c-kit and nanog, and c-kit and stem cell antigen (sca-1) were detected. The location of various types of cells within the cardio-annulation structure was observed. Adipogenic- and osteogenic-inducing fluids were used separately for in situ induction to detect the multidirectional differentiation potential of cells during the annulation process. After 3 to 6 days, cardiac cells migrated and formed an open or closed annulus with a diameter of 800 to 3500 µm. The annulus wall comprised the medial, middle, and lateral regions. The cells in the medial region were small, abundant, and laminated, while those in the middle region were larger with fewer layers, and those in the lateral region were less abundant, and loosely arranged in a single layer. Cardiomyocytes were distributed mainly on the surface of the medial region; nanog+ , c-kit+ , and sca-1+ cells were located mainly at the bottom of the annulus wall and fibroblasts were located mainly between these layers. The annulus cavity contained a large number of small, round cells, and telocytes. Cx43 was expressed in all cell types, and nanog, c-kit, and sca-1 were coexpressed in the cardio-annulation cells, which possess adipogenic and osteogenic differentiation potential. Cardio-annulation was discovered during an in vitro culture of cardiac cells. The structure contains cardiomyocytes, fibroblasts, telocytes, and abundant stem cells. These results provide insight into the relationship among cardiac cells in vitro.

Circular RNA 100146 functions as an oncogene through direct binding to miR-361-3p and miR-615-5p in non-small cell lung cancer.

Circular RNAs are widely expressed in eukaryotic cells and associated with cancer. However, limited studies to date have focused on the potential role of circRNAs in progression of lung cancer. Data from the current investigation showed that circRNA 100146 is highly expressed in non-small cell lung cancer (NSCLC) cell lines and the chemically induced malignant transformed bronchial cell line, 16HBE-T, as well as 40 paired tissue samples of NSCLC. Suppression of circRNA 100146 inhibited the proliferation and invasion of cells and promoted apoptosis. Furthermore, circRNA 100146 could interact with splicing factors and bind miR-361-3p and miR-615-5p to regulate multiple downstream mRNAs. Our collective findings support a role of circRNA 100146 in the development of NSCLC and further demonstrate endogenous competition among circRNA 100146, SF3B3 and miRNAs, providing novel insights into the mechanisms underlying non-small cell lung cancer.

Transcriptomic Responses of the Interactions between Clostridium cellulovorans 743B and Rhodopseudomonas palustris CGA009 in a Cellulose-Grown Coculture for Enhanced Hydrogen Production.

UNLABELLED: Coculturing dark- and photofermentative bacteria is a promising strategy for enhanced hydrogen (H2) production. In this study, next-generation sequencing was used to query the global transcriptomic responses of an artificial coculture of Clostridium cellulovorans 743B and Rhodopseudomonas palustris CGA009. By analyzing differentially regulated gene expression, we showed that, consistent with the physiological observations of enhanced H2 production and cellulose degradation, the nitrogen fixation genes in R. palustris and the cellulosomal genes in C. cellulovorans were upregulated in cocultures. Unexpectedly, genes related to H2 production in C. cellulovorans were downregulated, suggesting that the enhanced H2 yield was contributed mainly by R. palustris A number of genes related to biosynthesis of volatile fatty acids (VFAs) in C. cellulovorans were upregulated, and correspondingly, a gene that mediates organic compound catabolism in R. palustris was also upregulated. Interestingly, a number of genes responsible for chemotaxis in R. palustris were upregulated, which might be elicited by the VFA concentration gradient created by C. cellulovorans In addition, genes responsible for sulfur and thiamine metabolism in C. cellulovorans were downregulated in cocultures, and this could be due to a response to pH changes. A conceptual model illustrating the interactions between the two organisms was constructed based on the transcriptomic results. IMPORTANCE: The findings of this study have important biotechnology applications for biohydrogen production using renewable cellulose, which is an industrially and economically important bioenergy process. Since the molecular characteristics of the interactions of a coculture when cellulose is the substrate are still unclear, this work will be of interest to microbiologists seeking to better understand and optimize hydrogen-producing coculture systems.

Long-Term Enrichment on Cellulose or Xylan Causes Functional and Taxonomic Convergence of Microbial Communities from Anaerobic Digesters.

Cellulose and xylan are two major components of lignocellulosic biomass, which represents a potentially important energy source, as it is abundant and can be converted to methane by microbial action. However, it is recalcitrant to hydrolysis, and the establishment of a complete anaerobic digestion system requires a specific repertoire of microbial functions. In this study, we maintained 2-year enrichment cultures of anaerobic digestion sludge amended with cellulose or xylan to investigate whether a cellulose- or xylan-digesting microbial system could be assembled from sludge previously used to treat neither of them. While efficient methane-producing communities developed under mesophilic (35°C) incubation, they did not under thermophilic (55°C) conditions. Illumina amplicon sequencing results of the archaeal and bacterial 16S rRNA genes revealed that the mature cultures were much lower in richness than the inocula and were dominated by single archaeal (genus Methanobacterium) and bacterial (order Clostridiales) groups, although at finer taxonomic levels the bacteria were differentiated by substrates. Methanogenesis was primarily via the hydrogenotrophic pathway under all conditions, although the identity and growth requirements of syntrophic acetate-oxidizing bacteria were unclear. Incubation conditions (substrate and temperature) had a much greater effect than inoculum source in shaping the mature microbial community, although analysis based on unweighted UniFrac distance found that the inoculum still determined the pool from which microbes could be enriched. Overall, this study confirmed that anaerobic digestion sludge treating nonlignocellulosic material is a potential source of microbial cellulose- and xylan-digesting functions given appropriate enrichment conditions.

Regulation of cardiac fibroblasts reprogramming into cardiomyocyte-like cells with a cocktail of small molecule compounds.

Myocardial infarction results in extensive cardiomyocyte apoptosis, leading to the formation of noncontractile scar tissue. Given the limited regenerative capacity of adult mammalian cardiomyocytes, direct reprogramming of cardiac fibroblasts (CFs) into cardiomyocytes represents a promising therapeutic strategy for myocardial repair, and small molecule drugs might offer a more attractive alternative to gene editing approaches in terms of safety and clinical feasibility. This study aimed to reprogram rat CFs into cardiomyocytes using a small molecular chemical mixture comprising CHIR99021, Valproic acid, Dorsomorphin, SB431542, and Forskolin. Immunofluorescence analysis revealed a significant increase in the expression of cardiomyocyte-specific markers, including cardiac troponin T (cTnT), Connexin 43 (Cx43), α-actinin, and Tbx5. Changes in intracellular calcium ion levels and Ca2+ signal transfer between adjacent cells were monitored using a calcium ion fluorescence probe. mRNA sequencing analysis demonstrated the upregulation of genes associated with cardiac morphogenesis, myocardial differentiation, and muscle fiber contraction during CF differentiation induced by the small-molecule compounds. Conversely, the expression of fibroblast-related genes was downregulated. These findings suggest that chemical-induced cell fate conversion of rat CFs into cardiomyocyte-like cells is feasible, offering a potential therapeutic solution for myocardial injury.

The effects of inulin on solubilizing and improving anti-obesity activity of high polymerization persimmon tannin.

High polymerization persimmon tannin has been reported to have lipid-lowering effects. Unfortunately, the poor solubility restricts its application. This research aimed to investigate the effect and mechanism of inulin on solubilizing of persimmon tannin. Furthermore, we examined whether the addition of inulin would affect the attenuated obesity effect of persimmon tannin. Transmission electron microscope (TEM), Isothermal titration calorimetry (ITC) and Fourier transform infrared spectroscopy (FT-IR) results demonstrated that inulin formed a gel-like network structure, which enabled the encapsulation of persimmon tannin through hydrophobic and hydrogen bond interactions, thereby inhibiting the self-aggregation of persimmon tannin. The turbidity of the persimmon tannin solution decreased by 56.2 %, while the polyphenol content in the supernatant increased by 60.0 %. Furthermore, biochemical analysis and 16s rRNA gene sequencing technology demonstrated that persimmon tannin had a significant anti-obesity effect and improved intestinal health in HFD-fed mice. Moreover, inulin was found to have a positive effect on enhancing the health benefits of persimmon tannin, including improving hepatic steatosis and gut microbiota dysbiosis. it enhanced the abundance of beneficial core microbes while decreasing the abundance of harmful bacteria. Our findings expand the applications of persimmon tannin in the food and medical sectors.

Role of circPSEN1 in carbon black and cadmium co-exposure induced autophagy-dependent ferroptosis in respiratory epithelial cells.

Carbon black and cadmium (Cd) are important components of atmospheric particulate matter and cigarette smoke that are closely associated with the occurrence and development of lung diseases. Carbon black, particularly carbon black nanoparticles (CBNPs), can easily adsorbs metals and cause severe lung damage and even cell death. Therefore, this study aimed to explore the mechanisms underlying the combined toxicity of CBNPs and Cd. We found that the combined exposure to CBNPs and Cd promoted significantly greater autophagosome formation and ferroptosis (increased malonaldehyde (MDA), reactive oxygen species (ROS), and divalent iron ions (Fe2+) levels and altered ferroptosis-related proteins) compared with single exposure in both 16HBE cells (human bronchial epithelioid cells) and mouse lung tissues. The levels of ferroptosis proteins, transferrin receptor protein 1 (TFRC) and glutathione peroxidase 4 (GPX4), were restored by CBNPs-Cd exposure following treatment with a 3-MA inhibitor. Additionally, under CBNPs-Cd exposure, circPSEN1 overexpression inhibited increases in the autophagy proteins microtubule-associated protein 1 light chain 3 (LC3II/I) and sequestosome-1 (P62). Moreover, increases in TFRC and Fe2+, and decreases in GPX4were inhibited. Knockdown of circPSEN1 reversed these effects. circPSEN1 interacts with autophagy-related gene 5 (ATG5) protein and upregulates nuclear receptor coactivator 4 (NCOA4), the co-interacting protein of ATG5, thereby degrading ferritin heavy chain 1 (FTH1) and increasing Fe2+ in 16HBE cells. These results indicated that the combined exposure to CBNPs and Cd promoted the binding of circPSEN1 to ATG5, thereby increasing autophagosome synthesis and ATG5-NCOA4-FTH1 axis activation, ultimately inducing autophagy-dependent ferroptosis in 16HBE cells and mouse lung tissues. This study provides novel insights into the toxic effects of CBNPs and Cd in mixed pollutants.

Preparation methods and research progress of super-hydrophobic anti-icing surface.

The problem of surface icing poses a serious threat to people's economy and safety, especially in the fields of aerospace, wind power generation and circuit transmission. Super-hydrophobic has excellent anti-icing performance, so it has been widely studied. As the most promising anti-icing technology, superhydrophobic anti-icing surface should not only be simple to prepare, but also have excellent comprehensive performance, which can meet the anti-icing task under harsh working conditions and long-term durability. This paper summarizes the basic performance requirements of superhydrophobic surface for anti-icing operation, and then summarizes the preparation methods and existing problems of superhydrophobic surface in recent years. Finally, the future development trend of superhydrophobic anti-icing surface is prospected and discussed, hoping to provide certain technical guidance for the subsequent research of high-performance superhydrophobic anti-icing surface.

Circ_0008657 regulates lung DNA damage induced by hexavalent chromium through the miR-203a-3p/ATM axis.

Hexavalent chromium [Cr (VI)] is an important environmental pollutant and may cause lung injury when inhaled into the human body. Cr (VI) is genotoxic and can cause DNA damage, although the underlying epigenetic mechanisms remain unclear. To simulate the real-life workplace exposure to Cr (VI), we used a novel exposure dose calculation method. We evaluated the effect of Cr (VI) on DNA damage in human bronchial epithelial cells (16HBE and BEAS-2B) by calculating the equivalent real-time exposure dose of Cr (VI) (0 to 10 µM) in an environmental population. Comet experiments and olive tail moment measurements revealed increased DNA damage in cells exposed to Cr (VI). Cr (VI) treatment increased nuclear γ-H2AX foci and γ-H2AX protein expression, and caused DNA damage in the lung tissues of mice. An effective Cr (VI) dose (6 µM) was determined and used for cell treatment. Cr (VI) exposure upregulated circ_0008657, and knockdown of circ_0008657 decreased Cr (VI)-induced DNA damage, whereas circ_0008657 overexpression had the opposite effect. Mechanistically, we found that circ_0008657 binds to microRNA (miR)-203a-3p and subsequently regulates ATM serine/threonine kinase (ATM), a key protein involved in homologous recombination repair downstream of miR-203a-3p, thereby regulating DNA damage induced by Cr (VI). The present findings suggest that circ_0008657 competitively binds to miR-203a-3p to activate the ATM pathway and regulate the DNA damage response after environmental chemical exposure in vivo and in vitro.

Circ0087385 promotes DNA damage in benzo(a)pyrene-induced lung cancer development by upregulating CYP1A1.

Increasing environmental genotoxic chemicals have been shown to induce epigenetic alterations. However, the interaction between genetics and epigenetics in chemical carcinogenesis is still not fully understood. Here, we constructed an in vitro human lung carcinogenesis model (16HBE-T) by treating human bronchial epithelial cells with a typical significant carcinogen benzo(a)pyrene (BaP). We identified a novel circular RNA, circ0087385, which was overexpressed in 16HBE-T and human lung cancer cell lines, as well as in lung cancer tissues and serum exosomes from lung cancer patients. The upregulated circ0087385 after exposure to BaP promoted DNA damage in the early stage of chemical carcinogenesis and affected the cell cycle, proliferation, and apoptosis of the malignantly transformed cells. Overexpression of circ0087385 enhanced the expression of cytochrome P450 1A1 (CYP1A1), which is crucial for metabolically activating BaP. Interfering with circ0087385 or CYP1A1 reduced the levels of ultimate carcinogen benzo(a)pyrene diol epoxide (BPDE) and BPDE-DNA adducts. Interfering with CYP1A1 partially reversed the DNA damage induced by high expression of circ0087385, as well as decreased the level of BPDE and BPDE-DNA adducts. These findings provide novel insights into the interaction between epigenetics and genetics in chemical carcinogenesis which are crucial for understanding the epigenetic and genetic toxicity of chemicals.