K₂SO₄‑Assisted Hexagonal/Monoclinic WO₃ Phase Junction for Efficient Photocatalytic Degradation of RhB

Fabrication of a phase junction in the photocatalyst is one of the efficient strategies for enhancement of the photocatalytic activity. However, research on the relation between phase composition and photocatalytic property of WO₃ is limited because of the barely controllable phase transition process from monoclinic to hexagonal phase. A facile sol–gel synthesis of a composition tunable hexagonal/monoclinic-WO₃ (h/m-WO₃) phase junction with K₂SO₄ as stabilizing agent is developed. X-ray powder diffraction, scanning electron microscopy, UV–Raman, high-resolution transmission electron microscopy, and UV–vis diffusion reflectance spectroscopy are employed to investigate the structures, morphologies, crystalline phases, phase composition, and optical properties of the as-prepared samples. Contents of the hexagonal phase in the WO₃ samples can be precisely adjusted in a wide range from 0 to 71.1 wt % by regulating the K₂SO₄ amount, the calcination temperature, and the calcination time. Degradation of rhodamine B of samples indicates that the reaction rate depends significantly on the contents of the hexagonal/monoclinic phase in the WO₃ samples. A 7.4 times enhancement in the reaction rate is observed for the h/m-WO₃ sample with 71.1 wt % h-WO₃ than the pure m-WO₃. The increased photocatalytic activity is attributed to the formation of a phase junction between h-WO₃ and m-WO₃, which exhibits high efficiency of the separation and transfer of photoexcited electron–hole, as evident from electrochemical impedance spectra results. This work provides a new insight into the fabrication of a phase composition designable h/m-WO₃ phase junction with high photocatalytic performance, which benefits the application of WO₃ in environmental protection issues

Overexpression of miR-155 in the Liver of Transgenic Mice Alters the Expression Profiling of Hepatic Genes Associated with Lipid Metabolism

<div><p>Hepatic expression profiling has revealed miRNA changes in liver diseases, while hepatic miR-155 expression was increased in murine non-alcoholic fatty liver disease, suggesting that miR-155 might regulate the biological process of lipid metabolism. To illustrate the effects of miR-155 gain of function in transgenic mouse liver on lipid metabolism, transgenic mice (i.e., Rm155LG mice) for the conditional overexpression of mouse miR-155 transgene mediated by Cre/lox P system were firstly generated around the world in this study. Rm155LG mice were further crossed to Alb-Cre mice to realize the liver-specific overexpression of miR-155 transgene in Rm155LG/Alb-Cre double transgenic mice which showed the unaltered body weight, liver weight, epididymal fat pad weight and gross morphology and appearance of liver. Furthermore, liver-specific overexpression of miR-155 transgene resulted in significantly reduced levels of serum total cholesterol, triglycerides (TG) and high-density lipoprotein (HDL), as well as remarkably decreased contents of hepatic lipid, TG, HDL and free fatty acid in Rm155LG/Alb-Cre transgenic mice. More importantly, microarray data revealed a general downward trend in the expression profile of hepatic genes with functions typically associated with fatty acid, cholesterol and triglyceride metabolism, which is likely at least partially responsible for serum cholesterol and triglyceride lowering observed in Rm155LG/Alb-Cre mice. In this study, we demonstrated that hepatic overexpression of miR-155 alleviated nonalcoholic fatty liver induced by a high-fat diet. Additionally, carboxylesterase 3/triacylglycerol hydrolase (Ces3/TGH) was identified as a direct miR-155 target gene that is potentially responsible for the partial liver phenotypes observed in Rm155LG/Alb-Cre mice. Taken together, these data from miR-155 gain of function study suggest, for what we believe is the first time, the altered lipid metabolism and provide new insights into the metabolic state of the liver in Rm155LG/Alb-Cre mice.</p></div

Blood profile for control and Rm155LG/Alb-Cre mice.

<p>Cre control mice were littermates of the Rm155LG/Alb-Cre mice. Aspartate aminotransferase (AST), alanine transaminase (ALT), cholesterol and triglyceride values were determined in serum. WAT, white adipose tissue; TC, total cholesterol; TG, triglycerides; LDL, low-density lipoprotein; HDL, high-density lipoprotein. Data are mean ± SD. Statistical significance was determined by two-tailed student t-test.</p><p>*, <i>P</i><0.05.</p><p>Blood profile for control and Rm155LG/Alb-Cre mice.</p

Rm155LG/Alb-Cre mice improved lipid metabolism in liver.

<p>(<b>A</b>) Body weight of Rm155LG/Alb-Cre mice and controls at different ages. (<b>B</b>) Relative liver weight of Rm155LG/Alb-Cre mice vs. controls. (<b>C</b>) Adult Rm155LG/Alb-Cre mouse (right) and control (left) fed a normal diet. (<b>D</b>) Gross morphology of Rm155LG/Alb-Cre mouse (right) and control (left) livers. <b>(E)</b> H&E staining and Oil red O (ORO) staining of liver sections from control and Rm155LG/Alb-Cre mice. (<b>F</b>) Quantification of TC, TG, HDL and FFA storage in the liver of control and Rm155LG/Alb-Cre mice. TC, total cholesterols; TG, triglycerides; HDL, high-density lipoprotein; FFA, free fatty acids. Data are mean±SD (n = 9–10). Statistical significance was determined by two-tailed student t-test.</p

Microarray revealed the altered hepatic lipid metabolism genes in the liver of Rm155LG/Alb-Cre mice.

<p>(<b>A</b>) Class comparison and hierarchical clustering of differentially expressed hepatic lipid metabolism-related genes between Rm155LG/Alb-Cre and control mouse liver. A cluster heat map for hepatic lipid metabolism-related genes (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s010" target="_blank">S6 Table</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s011" target="_blank">S7 Table</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s012" target="_blank">S8 Table</a>) is shown. Other details as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s002" target="_blank">S2 Fig</a>. (<b>B-C</b>) Gene ontology (GO) (B) and KEGG pathway (C) analyses of up- and down-regulated genes between Rm155LG/Alb-Cre and control mouse liver. Genes with expression changes of greater than 2-fold with P values below 0.05 were identified and classified using GO categories.</p

Enforced expression of miR-155 in the liver of Rm155LG/Alb-Cre mice improved HFD-induced hepatic steatosis.

<p><b>(A)</b> Body weight of Rm155LG/Alb-Cre mice and controls fed normal chow diet or HFD. <b>(B)</b> Liver weight of Rm155LG/Alb-Cre mice vs. controls fed normal chow diet or HFD. <b>(C)</b> H&E staining and ORO staining of liver sections from control and Rm155LG/Alb-Cre mice. <b>(D-G)</b> Quantification of TC and TG in the serum and liver of control and Rm155LG/Alb-Cre mice fed either chow diet or HFD. Data are mean±SD (n = 6–8). Other details as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.g003" target="_blank">Fig. 3</a>.</p

Identification of Ces3/TGH as a miR-155 target gene.

<p><b>(A)</b> Ces3 is a target gene of miR-155. The luciferase reporter assay was performed using Hepa1–6 cells as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#sec002" target="_blank">Materials and methods</a> section. <b>(B)</b> Microarray revealed the reduced expression of Ces3 in the liver of Rm155LG/Alb-Cre mice. A cluster heat map for 9 hepatic lipid metabolism-related genes is shown. Other details as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s002" target="_blank">S2 Fig</a>. <b>(C)</b> qRT-PCR analysis of Ces3 expression in Rm155LG/Alb-Cre mouse liver. <b>(D-E)</b> qRT-PCR assay for Ces3 expression in vector- and miR-155-expressing 7402 (D) and 7404 (E) cells. <b>(F)</b> qRT-PCR analysis of Ces3 expression in miR-155 knockout mouse liver. <b>(G)</b> Schematic diagram indicating the pathway of miR-155-mediated downregulation of Ces3 expression leading to reduced hepatic and blood TG levels.</p

A proposed model on miR-155 overexpression reducing hepatic and blood lipid profiles.

<p>The enforced expression of miR-155 in the liver of transgenic mice is able to induce a general downward trend in the expression profile of hepatic genes involved lipogenesis, fatty acid metabolism, triacylglycerol metabolism, cholesterol metabolismn and bile acid biosynthesis, etc, thereby causing the decreased hepatic lipid content by decreasing adipogenic and lipogenic gene expression in liver, which reduces blood lipid concentration. Other details as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s010" target="_blank">S6 Table</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s011" target="_blank">S7 Table</a>.</p

cDNA microarray and qRT-PCR revealed a general downward trend in the expression of hepatic cholesterol, triacylglycerol and fatty acid synthesis-related genes in Rm155LG/Alb-Cre transgenic mouse liver.

<p>Graph illustrating the fold change in gene expression of representative differentially hepatic lipid metabolism-related genes between Rm155LG/Alb-Cre and control mouse liver. qRT-PCR validated microarray-derived data on the increased or decreased mRNA expression of hepatic lipid metabolism-related genes in Rm155LG/Alb-Cre transgenic mouse liver. Additionally, a cluster heat map for hepatic lipid metabolism-related genes (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s010" target="_blank">S6 Table</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s011" target="_blank">S7 Table</a>) is shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.g004" target="_blank">Fig. 4A</a>. Other details as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118417#pone.0118417.s002" target="_blank">S2 Fig</a>.</p