Genome-Engineered mpkCCDc14 Cells as a New Resource for Studying AQP2.

mpkCCDc14 cells, a polarized epithelial cell line derived from mouse kidney cortical collecting ducts, are known to express the vasopressin V2 receptor (V2R) and aquaporin-2 (AQP2) that are responsive to vasopressin. However, a low abundance of the endogenous AQP2 protein in the absence of vasopressin and heterogeneity of AQP2 protein abundance among the cultured cells may limit the further application of the cell line in AQP2 studies. To overcome the limitation, we aimed to establish mpkCCDc14 cells constitutively expressing V2R and AQP2 via CRISPR/Cas9-mediated genome engineering technology (i.e., V2R-AQP2 cells). 3'- and 5'-Junction PCR revealed that the V2R-AQP2 expression cassette with a long insert size (~2.2 kb) was correctly integrated. Immunoblotting revealed the expression of products of integrated Aqp2 genes. Cell proliferation rate and dDAVP-induced cAMP production were not affected by the knock-in of Avpr2 and Aqp2 genes. The AQP2 protein abundance was significantly higher in V2R-AQP2 cells compared with control mpkCCDc14 cells in the absence of dDAVP and the integrated AQP2 was detected. Immunocytochemistry demonstrated that V2R-AQP2 cells exhibited more homogenous and prominent AQP2 labeling intensity in the absence of dDAVP stimulation. Moreover, prominent AQP2 immunolabeling (both AQP2 and pS256-AQP2) in the apical domain of the genome-edited cells was observed in response to dDAVP stimulation, similar to that in the unedited control mpkCCDc14 cells. Taken together, mpkCCDc14 cells constitutively expressing V2R and AQP2 via genome engineering could be exploited for AQP2 studies.

A nonbiodegradable scaffold-free cell sheet of genome-engineered mesenchymal stem cells inhibits development of acute kidney injury.

Cell therapy using genome-engineered stem cells has emerged as a novel strategy for the treatment of kidney diseases. By exploiting genome editing technology, human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) secreting an angiogenic factors or an anti-inflammatory factor were generated for therapeutic application in acute kidney injury. Junction polymerase chain reaction analysis verified zinc finger nucleases-assisted integration of the desired gene into the hUC-MSCs. Flow cytometry and differentiation assays indicated that genome editing did not affect the differentiation potential of these mesenchymal stem cells. Protein measurement in conditioned media with the use of ELISA and immunoblotting revealed the production and secretion of each integrated gene product. For cell therapy in the bilateral ischemia-reperfusion mouse model of acute kidney injury, our innovative scaffold-free cell sheets were established using a non-biodegradable temperature-responsive polymer. One of each type of scaffold-free cell sheets of either the angiogenic factor vascular endothelial grown factor or angiopoietin-1, or the anti-inflammatory factor erythropoietin, or α-melanocyte-stimulating hormone-secreting hUC-MSCs was applied to the decapsulated kidney surface. This resulted in significant amelioration of kidney dysfunction in the mice with acute kidney injury, effects that were superior to intravenous administration of the same genome-engineered hUC-MSCs. Thus, our scaffold-free cell sheets of genome-engineered mesenchymal stem cells provides therapeutic effects by inhibiting acute kidney injury via angiogenesis or anti-inflammation.

Exosomes co-expressing AQP5-targeting miRNAs and IL-4 receptor-binding peptide inhibit the migration of human breast cancer cells.

Aquaporin-5 (AQP5) plays a role in breast cancer cell migration. This study aimed to identify AQP5-targeting miRNAs and examine their effects on breast cancer cell migration through exosome-mediated delivery. Bioinformatic analyses identified miR-1226-3p, miR-19a-3p, and miR-19b-3p as putative regulators of AQP5 mRNA. Immunoblotting revealed a decrease of AQP5 protein abundance when each of these miRNAs was transfected into human breast cancer MDA-MB-231 cells. Quantitative real-time PCR demonstrated the reduction of AQP5 mRNA expression by the transfection of miR-1226-3p and a luciferase reporter assay revealed the reduction of AQP5 translation after the transfection of miR-19b-3p in MDA-MB-231 cells. Consistently, the transfection of each miRNA impeded cell migration. Pathway enrichment analyses showed that these three miRNAs regulate target genes, which were predominantly enriched in the gap junction pathway. For the efficient delivery of AQP5-targeting miRNAs to breast cancer cells, exosomes expressing both miRNAs and a peptide targeting interleukin-4 receptor, which is highly expressed in breast cancer cells, were bioengineered and their inhibitory effects on AQP5 protein expression and cell migration were demonstrated in MDA-MB-231 cells. Taken together, AQP5-regulating miRNAs are identified, which could be exploited for the inhibition of breast cancer cell migration via the exosome-mediated delivery.

miR-34c-5p and CaMKII are involved in aldosterone-induced fibrosis in kidney collecting duct cells.

Mineralocorticoids trigger a profibrotic process in the kidney. In mouse cortical collecting duct cells, the present study addressed two main questions: 1) what are microRNAs (miRNAs) and their target genes that are changed by aldosterone? and 2) what do miRNAs, in response to aldosterone, regulate regarding signaling pathways related to fibrosis? A microarray chip assay was done in cells in the absence or presence of aldosterone treatment (10-6 M; 3 days). The candidate miRNAs were identified by the criteria of >30% of fold change among the significantly changed miRNAs ( P < 0.05). Twenty-nine miRNAs were upregulated (>1.3-fold), and 27 miRNAs were downregulated (<0.7-fold). Putative target genes of identified miRNAs were associated with 74 Kyoto Encyclopedia of Genes and Genomes pathways. Among them, the wingless-related integration site (Wnt) signaling pathway was highly ranked, where 15 mature miRNAs were observed. These miRNAs were further analyzed by real-time quantitative PCR, and among them, miR-130b-3p, miR-34c-5p, and miR-146a-5p were selected. Through the identification of putative target genes of these three miRNAs, mRNA and protein expression of the Ca2+/calmodulin-dependent protein kinase type II ß-chain ( Camk2b) gene (a target gene of miR-34c-5p) were found to be increased significantly in aldosterone-treated cells, where fibronectin (FN) and α-smooth muscle actin were induced. When CaMKIIß small interfering RNA or the miR-34c-5p mimic was transfected, aldosterone-induced FN expression was significantly attenuated, along with reduced CaMKIIß protein expression. A luciferase reporter assay revealed a decrease of CaMKIIß translation in cells transfected with miRNA mimics of miR-34c-5p. In conclusion, aldosterone-induced downregulation of miR-34c-5p in the Wnt signaling pathway and a consequent increase of CaMKIIß expression are likely to be involved in aldosterone-induced fibrosis.

CK2α/CSNK2A1 Phosphorylates SIRT6 and Is Involved in the Progression of Breast Carcinoma and Predicts Shorter Survival of Diagnosed Patients.

Recently, the roles of sirtuins (SIRTs) in tumorigenesis have been of interest to oncologists, and protein kinase CK2 α1 (CSNK2A1) has been shown to be involved in tumorigenesis by phosphorylating various proteins, including SIRT1. Therefore, we evaluated the roles of CSNK2A1, SIRT6, and phosphorylated SIRT6 and their relationships in breast carcinoma. Nuclear expression of CSNK2A1 and SIRT6 predicted shorter overall survival and relapse-free survival by multivariate analysis. Inhibition of CSNK2A1 decreased the proliferative and invasive activity of cancer cells. In addition, CSNK2A1 was bound to SIRT6 and phosphorylated SIRT6; evidence for this is provided from immunofluorescence staining, co-immunoprecipitation of CSNK2A1 and SIRT6, a glutathione S-transferase pull-down assay, an in vitro kinase assay, and transfection of mutant CSNK2A1. Knockdown of SIRT6 decreased the proliferation and invasiveness of cancer cells. Overexpression of SIRT6 increased proliferation, but mutation at the Ser338 phosphorylation site of SIRT6 inhibited the proliferation of MCF7 cells. Moreover, both knockdown of SIRT6 and a mutation at the phosphorylation site of SIRT6 decreased expression of matrix metallopeptidase 9, ß-catenin, cyclin D1, and NF-κB. Especially, SIRT6 expression was associated with the nuclear localization of ß-catenin. This study demonstrates that CSNK2A1 and SIRT6 are indicators of poor prognosis for breast carcinomas and that CSNK2A1-mediated phosphorylation of SIRT6 might be involved in the progression of breast carcinoma.

Protection against RAGE-mediated neuronal cell death by sRAGE-secreting human mesenchymal stem cells in 5xFAD transgenic mouse model.

Alzheimer's disease (AD), which is the most commonly encountered neurodegenerative disease, causes synaptic dysfunction and neuronal loss due to various pathological processes that include tau abnormality and amyloid beta (Aß) accumulation. Aß stimulates the secretion and the synthesis of Receptor for Advanced Glycation End products (RAGE) ligand by activating microglial cells, and has been reported to cause neuronal cell death in Aß1-42 treated rats and in mice with neurotoxin-induced Parkinson's disease. The soluble form of RAGE (sRAGE) is known to reduce inflammation, and to decrease microglial cell activation and Aß deposition, and thus, it protects from neuronal cell death in AD. However, sRAGE protein has too a short half-life for therapeutic purposes. We developed sRAGE-secreting umbilical cord derived mesenchymal stem cells (sRAGE-MSCs) to enhance the inhibitory effects of sRAGE on Aß deposition and to reduce the secretion and synthesis of RAGE ligands in 5xFAD mice. In addition, these cells improved the viability of injected MSCs, and enhanced the protective effects of sRAGE by inhibiting the binding of RAGE and RAGE ligands in 5xFAD mice. These findings suggest sRAGE protein from sRAGE-MSCs has better protection against neuronal cell death than sRAGE protein or single MSC treatment by inhibiting the RAGE cell death cascade and RAGE-induce inflammation.

Depletion of vacuolar protein sorting-associated protein 35 is associated with increased lysosomal degradation of aquaporin-2.

The carboxyl terminus of aquaporin-2 (AQP2c) undergoes posttranslational modifications, including phosphorylation and ubiquitination, in the process of regulating aquaporin-2 (AQP2) translocation and protein abundance. We aimed to identify novel proteins interacting with AQP2c. Recombinant AQP2c protein was made in Escherichia coli BL21 (DE3) cells by exploiting the pET32 TrxA fusion system. Lysates of rat kidney inner medullary collecting duct (IMCD) tubule suspensions interacted with rat AQP2c bound to Ni2+-resin were subjected to LC-MS/MS proteomic analysis. Potential interacting proteins were identified, including vacuolar protein sorting-associated protein 35 (Vps35). Coimmunoprecipitation assay demonstrated that Vps35 interacted with AQP2c. Immunohistochemistry of rat kidney revealed that AQP2 and Vps35 were partly colocalized at the intracellular vesicles in collecting duct cells. The role of Vps35 in AQP2 regulation induced by 1-deamino-8D-arginine vasopressin (dDAVP) was examined in mpkCCDc14 cells. Cell surface biotinylation assay demonstrated that dDAVP-induced apical translocation of AQP2 was significantly decreased under siRNA-mediated Vps35 knockdown. dDAVP-induced AQP2 upregulation was less prominent in the cells with Vps35 knockdown. Moreover, AQP2 protein abundance was decreased to a greater extent during the withdrawal period after dDAVP stimulation under Vps35 knockdown, which was significantly inhibited by chloroquine (a blocker of the lysosomal pathway) but not by MG132 (a proteasome inhibitor). Immunocytochemistry demonstrated that internalized AQP2 was more associated with lysosomal-associated membrane protein 1 (LAMP-1) in primary cultured IMCD cells under a Vps35 knockdown situation. Taken together, our results show that Vps35 interacts with AQP2c, and depletion of Vps35 is likely to be associated with decreased AQP2 trafficking and increased lysosomal degradation of AQP2 protein.

Association of low baseline free thyroxin levels with progression of coronary artery calcification over 4 years in euthyroid subjects: the Kangbuk Samsung Health Study.

OBJECTIVE: Overt and subclinical hypothyroidism are risk factors for atherosclerosis and cardiovascular diseases. It is unclear whether thyroid hormone levels within the normal range are also associated with atherosclerosis measured by coronary artery calcium (CAC). CONTEXT: This study aimed to examine the relationship between normal variations in thyroid function and changes in CAC. MEASUREMENTS: We conducted a 4-year retrospective study of 2173 apparently healthy men and women with normal thyroid hormone levels. Their free thyroxin (FT4), free triiodothyronin (FT3) and thyroid-stimulating hormone (TSH) levels were measured by electrochemiluminescent immunoassay. The CAC score (CACS) of each subject was measured by multidetector computed tomography in both 2010 and 2014. Progression of CAC was defined as a CACS change over 4 years > 0. RESULTS: The mean CACS changes over 4 years by quartiles of baseline FT4 level (lowest to highest) were 12·9, 8·43, 7·82 and 7·81 (P = 0·028). CAC progression was not significantly associated with either the baseline FT3 or TSH levels. The odds ratios (OR) for CAC progression over 4 years (highest vs lowest quartile for baseline FT4) were 0·647 (95% confidence interval (CI) 0·472-0·886) after adjustment for confounding factor, which were attenuated with further adjustment for lipid profiles, homoeostasis model assessment of insulin resistance, high-sensitivity C-reactive protein and hypertension [0·747 (95% CI 0·537-1·038)]. Quartiles of baseline FT3 or TSH level did not show any increased OR for CAC progression after adjustment for confounding factors. CONCLUSIONS: In this cohort of euthyroid men and women, a low baseline FT4 level was associated with a high risk of CACS progression over 4 years.

The relationship between serum fatty-acid binding protein 4 level and lung function in Korean subjects with normal ventilatory function.

BACKGROUND: The aim of this study was to assess the association of lung function with serum fatty-acid binding protein 4 (FABP4) in apparently healthy Korean adults. METHODS: In 495 participants in a health screening program, Force Exploratory Volume (FEV) 1 and Forced Vital Capacity (FVC) were assessed with standard spirometry. Subjects with obstructive (n = 19) and restrictive (n = 45) lung function were excluded from the analysis. Serum FABP4 level was measured by enzyme-linked immunosorbent assay and transformed into Ln(FABP4). 431 subjects with normal ventilator function (72.4% men, mean age 41 years) were included in the final analysis. RESULTS: Mean Ln(FABP4) significantly decreased in subjects from 1(st) quartile to 4(th) quartile of FVC (p = 0.008). Ln(FABP4) did not show significant differences across the quartile groups of FEV1. The odds ratio (OR) of being in the lowest quartile of FVC was 2.704 in subject with 3(rd) tertile of Ln(FABP4) after full adjustment for confounding variables {95% confidence interval (CI) 1.397 ~ 5.357}. OR of being in the lowest quartile of FEV1 was 1.822 (95% CI 1.021 ~ 3.298) in subjects with 3(rd) tertile of Ln(FABP4) after adjustment of age and sex, which was attenuated after full adjustment for confounding variables. CONCLUSION: Increased FABP4 level showed increased risk for reduced lung function in subjects with normal ventilatory function.

Introduction of functionality, selection of topology, and enhancement of gas adsorption in multivariate metal-organic framework-177.

Metal-organic framework-177 (MOF-177) is one of the most porous materials whose structure is composed of octahedral Zn4O(-COO)6 and triangular 1,3,5-benzenetribenzoate (BTB) units to make a three-dimensional extended network based on the qom topology. This topology violates a long-standing thesis where highly symmetric building units are expected to yield highly symmetric networks. In the case of octahedron and triangle combinations, MOFs based on pyrite (pyr) and rutile (rtl) nets were expected instead of qom. In this study, we have made 24 MOF-177 structures with different functional groups on the triangular BTB linker, having one or more functionalities. We find that the position of the functional groups on the BTB unit allows the selection for a specific net (qom, pyr, and rtl), and that mixing of functionalities (-H, -NH2, and -C4H4) is an important strategy for the incorporation of a specific functionality (-NO2) into MOF-177 where otherwise incorporation of such functionality would be difficult. Such mixing of functionalities to make multivariate MOF-177 structures leads to enhancement of hydrogen uptake by 25%.

Higher association of coronary artery calcification with non-alcoholic fatty liver disease than with abdominal obesity in middle-aged Korean men: the Kangbuk Samsung Health Study.

BACKGROUND: It is uncertain whether non-alcoholic fatty liver disease (NAFLD) or abdominal obesity is more associated with atherosclerosis. The aim of this study was to determine whether NAFLD or abdominal obesity is more strongly associated with subclinical atherosclerosis represented by coronary artery calcification (CAC). METHODS: A total of 21,335 male participants in a health screening program (mean age 41 years) were enrolled. Ultrasonographic measurements of fatty liver and multi-detector computed tomography were performed to determine the coronary artery calcium score (CACS). The presence of CAC was defined as CACS > 0. Subjects were divided into four groups according to the presence or absence of NAFLD and/or abdominal obesity as assessed by waist-hip ratio (WHR) > 0.9. RESULTS: The presence of CAC was detected in 2,385 subjects (11.2%). The proportion of subjects with CAC was highest in the abdominal obesity only group (23.2%). After adjustment for age, diabetes history, hypertension, cigarette smoking, and physical inactivity, the odds ratio (OR) for CAC was the highest in the group with both abnormalities [1.465 (1.324-1.623)]. The NAFLD only group showed significantly increased OR for CAC compared to that in the abdominal obesity only group [1.286 (1.151-1.436) vs. 1.076 (0.939-1.233)]. CONCLUSION: Non-alcoholic fatty liver disease is more closely associated with CAC than abdominal obesity as assessed by the WHR. NAFLD could be considered an independent determinant of subclinical atherosclerosis as assessed by CAC.

Teriparatide therapy for bisphosphonate-related osteonecrosis of the jaw associated with dental implants.

This report describes a case of teriparatide (TPTD) therapy for bisphosphonate (BP)-related osteonecrosis of the jaw induced after implant placement. A 75-year-old woman taking oral BP was referred with uncontrolled osteonecrosis of the mandible related to the implant placement. With conservative treatment, BP was suspended and daily subcutaneous injections of 20 µm/d TPTD were started. After 4 months of the therapy, fixture removal and sequestrectomy were performed. Histological analysis revealed necrotic lamellar bone and empty osteocytic lacunae. In contrast, multiple irregular reversal lines of the lamellar bone and active osteoblasts were noted adjacent to the lesion. There was a significant increase in serum C-terminal telopeptide cross-link of type 1 collagen and serum osteocalcin after commencement of the therapy. After 7 months off therapy, the serum levels of the 2 markers remained at a high level compared with the baseline.

Quality and composition of archived nucleic acids after use in SARS-CoV-2 molecular testing.

BACKGROUND: Reverse transcription real-time PCR (rRT-PCR) has been a gold-standard method to detect SARS-CoV-2, for which quality assessment of nucleic acids (NAs) is not needed. In order to prepare for future use, we evaluated NA quality from archived SARS-CoV-2 rRT-PCR samples. METHODS: NA samples were collected in February 2021 and extracted using the QIAamp DSP Virus Spin Kit, (53 SARS-CoV-2-positive and 100 SARS-CoV-2-negative). Quality, quantity, and purity of NA were measured spectrophotometrically or fluorescently. Droplet digital PCR was used to characterize the double strand DNA (dsDNA) origin and composition by quantifying 16S rDNA and RPP30. RESULTS: The RIN and purity were not significantly different between groups (p = 0.3828). RNA quantity was significantly higher than dsDNA in both groups (p < 0.0001); both dsDNA and RNA quantity were significantly higher in positive samples (dsDNA, RNA p = 0.021). For dsDNA, 16S rDNA copies were significantly greater than RPP30 in both groups (p < 0.0001), and RPP30 were significantly higher in positive samples (p < 0.0001). CONCLUSIONS: Archived NA quality after SARS-CoV-2 rRT-PCR was guaranteed for subsequent molecular research using human or bacterial DNA, especially for short targets.

Comparison of gas sorption properties of neutral and anionic metal-organic frameworks prepared from the same building blocks but in different solvent systems.

Two different 3D porous metal-organic frameworks, [Zn4O(NTN)2]·10DMA·7H2O (SNU-150) and [Zn5(NTN)4(DEF)2][NH2(C2H5)2]2·8DEF·6H2O (SNU-151), are synthesized from the same metal and organic building blocks but in different solvent systems, specifically, in the absence and the presence of a small amount of acid. SNU-150 is a doubly interpenetrated neutral framework, whereas SNU-151 is a non-interpenetrated anionic framework containing diethylammonium cations in the pores. Comparisons of the N2, H2, CO2, and CH4 gas adsorption capacities as well as the CO2 adsorption selectivity over N2 and CH4 in desolvated SNU-150' (BET: 1852 m(2) g(-1)) and SNU-151' (BET: 1563 m(2) g(-1)) samples demonstrate that the charged framework is superior to the neutral framework for gas storage and gas separation, despite its smaller surface area and different framework structure.

Mercury induces the expression of cyclooxygenase-2 and inducible nitric oxide synthase.

Nuclear factor-κB (NF-κB) is a transcription factor that mediates the inducible expression of a variety of genes involved in immune and inflammatory responses. NF-κB activation induces numerous proinflammatory gene products including cytokines, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). The divalent heavy metal mercury has been used for thousands of years. Although mercury is clearly toxic to most mammalian organ systems, especially the immune system, exposure has still increased in some areas of the world. However, the underlying toxic mechanism is not clearly identified. Here, we report biochemical evidence that mercury alone induces NF-κB activation, resulting in the induced expression of COX-2 and iNOS. The results suggest that mercury can induce inflammatory diseases by lowering host defense.

Reducing Microbial Contamination in Hematopoietic Stem Cell Products and Quality Improvement Strategy: Retrospective Analysis of 1996-2021 Data.

Background: Sterility and safety assurance of hematopoietic stem cell (HSC) products is critical in transplantation. Microbial contamination can lead to product disposal and increases the risk of unsuccessful clinical outcomes. Therefore, it is important to implement and maintain good practice guidelines and regulations for the HSC collection and processing unit in each hospital. We aimed to share our experiences and suggest strategies to improve the quality assurance of HSC processing. Methods: We retrospectively analyzed microbial culture results of 11,743 HSC products processed over a 25-year period (January 1996 to May 2021). Because of reorganization of the HSC management system in 2008, the 25-year period was divided into periods 1 (January 1996 to December 2007) and 2 (January 2008 to May 2021). We reviewed all culture results of the HSC products and stored aliquot samples and collected culture results for peripheral blood and catheter samples. Results: Of the 11,743 products in total, 35 (0.3%) were contaminated by microorganisms, including 19 (0.5%) of 3,861 products during period 1 and 16 (0.2%) of 7,882 products during period 2. Penicillium was the most commonly identified microorganism (15.8%) during period 1 and coagulase-negative Staphylococcus was the most commonly identified (31.3%) during period 2. HSC product contamination occurred most often during HSC collection and processing. Conclusions: The contamination rate decreased significantly during period 2, when the HSC management system was reorganized. Our results imply that handling HSC products by trained personnel and adopting established protocols, including quality assurance programs, aid in decreasing the contamination risk.

Histone methyltransferase SETD3 regulates muscle differentiation.

Histone lysine methylation, as one of the most important factors in transcriptional regulation, is associated with a various physiological conditions. Using a bioinformatics search, we identified and subsequently cloned mouse SET domain containing 3 (SETD3) with SET (Su(var)3-9, Enhancer-of-zeste and Trithorax) and Rubis-subs-bind domains. SETD3 is a novel histone H3K4 and H3K36 methyltransferase with transcriptional activation activity. SETD3 is expressed abundantly in muscular tissues and, when overexpressed, activates transcription of muscle-related genes, myogenin, muscle creatine kinase (MCK), and myogenic factor 6 (Myf6), thereby inducing muscle cell differentiation. Conversely, knockdown of SETD3 by shRNA significantly retards muscle cell differentiation. In this study, SETD3 was recruited to the myogenin gene promoter along with MyoD where it activated transcription. Together, these data indicate that SETD3 is a H3K4/K36 methyltransferase and plays an important role in the transcriptional regulation of muscle cell differentiation.

Inverted organic solar cells with ZnO nanowalls prepared using wet chemical etching in a KOH solution.

We report on the photovoltaic (PV) performances of inverted organic solar cells (IOSCs) that were fabricated from PCBM:P3HT polymer with a ZnO thin film and ZnO nanowalls as electron transport and hole block layers. ZnO thin film on ITO/glass substrate was deposited using a simply aqueous solution route. ZnO nanowall structures were obtained via wet chemical etching of ZnO thin films in a KOH solution. The power conversion efficiency (PCE) of the IOSC with ZnO nanowalls was significantly improved by 44% from 1.254% to 1.811% compared to that of the IOSC with ZnO thin film. The short circuit current in IOSCs fabricated with the ZnO nanowalls was increased mainly due to the increase in the charge transport interface area, as a result of enhancement in the PCE. This work suggests a method for fabricating efficient PV devices with a larger charge transport area for future prospects.

Anti­inflammatory effects of Nypa fruticans Wurmb via NF­κB and MAPK signaling pathways in macrophages.

The inflammatory defense response of macrophages is a natural protective reaction in the immune system. Antioxidant and anti-inflammatory activities are closely related. In addition, the cell signaling pathway regulating inflammation is associated with MAPK and NF-κB signaling pathway phosphorylation. The present study aimed to evaluate whether the ethyl acetate fraction from N. fruticans (ENF) has a modulatory role in the MAPK signaling pathway and inhibition of the IκB/NF-κB signaling pathways, including translocation of NF-κB p65. Antioxidant and anti-inflammatory activities are closely related. In addition, the cell signaling pathway regulating inflammation is associated with MAPK and NF-κB signaling pathway phosphorylation. The results revealed that ENF exhibited antioxidant capacity, attenuated the cytokine levels and blocked nitric oxide production. ENF downregulated cyclooxygenase-2 and inducible nitric oxide synthase expression. We hypothesized that ENF treatment alleviated the various proinflammatory mediators via IκB phosphorylation and transcription of NF-κB compared with the untreated control. In conclusion, the present study demonstrated that the inhibitory effect of ENF treatment was attributed to the inhibition of MAPK and Akt/IκB/NF-κB signaling pathways.