Expression of the transcription factor regulatory factor X1 in the mouse brain

Limited information indicates that the regulatory factor X1 (RFX1), the prototype member of the transcription factor RFX family, may play a role in the central nervous system. Our recent study showed that knockout of the Rfx1 gene led to early embryonic death. In the present study, we showed that heterozygous Rfx1+/– mice were fertile and grew normally. An abundant amount of RFX1 proteins were expressed in the olfactory bulb, hippocampus and cerebral cortex as detected by b-galactosidase staining (the gene knockout vector contained a coding region for b-galactosidase) and immunofluorescent staining with an anti-RFX1 antibody. RFX1 positive immunostaining was mainly in the nuclei of neurons and microglial cells and was absent from the astrocytes of mouse brains. The heterozygous Rfx1+/– mice expressed RFX1 mRNA and proteins at a level similar to that in the wild-type mice in the olfactory bulb and hippocampus. The expression level of RFX1 proteins was similar in the brains of mice ranging from 15 day old embryos to four month old adults. Our results suggest a significant expression of RFX1 proteins in the mammalian brain. This expression is cell-type and brain-region specific and may take a random monoallelic expression pattern. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 2, pp. 344–351

Lentiviral-Mediated shRNA Silencing of PDE4D Gene Inhibits Platelet-Derived Growth Factor-Induced Proliferation and Migration of Rat Aortic Smooth Muscle Cells

Phosphodiesterase 4D (PDE4D) is a member of the large superfamily of phosphodiesterases. PDE4D polymorphisms have been found to associate with ischemic stroke. Proliferation and migration of vascular smooth muscle cells (VSMCs) play a critical role in the pathogenesis of atherosclerosis. In this study, infection of VSMCs with lentivrius particles carrying shRNA direct against PDE4D significantly inhibited platelet-derived growth factor-induced VSMC proliferation and migration, and the inhibitory effects were not associated with global intracellular cAMP level. Our results implicate that PDE4D has an important role in VSMC proliferation and migration which may explain its genetic susceptibility to ischemic stroke

Capping protein modulates the dynamic behavior of actin filaments in response to phosphatidic Acid in Arabidopsis.

International audienceRemodeling of actin filament arrays in response to biotic and abiotic stimuli is thought to require precise control over the generation and availability of filament ends. Heterodimeric capping protein (CP) is an abundant filament capper, and its activity is inhibited by membrane signaling phospholipids in vitro. How exactly CP modulates the properties of filament ends in cells and whether its activity is coordinated by phospholipids in vivo is not well understood. By observing directly the dynamic behavior of individual filament ends in the cortical array of living Arabidopsis thaliana epidermal cells, we dissected the contribution of CP to actin organization and dynamics in response to the signaling phospholipid, phosphatidic acid (PA). Here, we examined three cp knockdown mutants and found that reduced CP levels resulted in more dynamic activity at filament ends, and this significantly enhanced filament-filament annealing and filament elongation from free ends. The cp mutants also exhibited more dense actin filament arrays. Treatment of wild-type cells with exogenous PA phenocopied the actin-based defects in cp mutants, with an increase in the density of filament arrays and enhanced annealing frequency. These cytoskeletal responses to exogenous PA were completely abrogated in cp mutants. Our data provide compelling genetic evidence that the end-capping activity of CP is inhibited by membrane signaling lipids in eukaryotic cells. Specifically, CP acts as a PA biosensor and key transducer of fluxes in membrane signaling phospholipids into changes in actin cytoskeleton dynamics

Stanniocalcin 2 Ameliorates Hepatosteatosis Through Activation of STAT3 Signaling

Stanniocalcin 2 (STC2), a secreted glycoprotein hormone, regulates many biological processes, including cell proliferation, apoptosis, tumorigenesis, and atherosclerosis. However, its role in hepatic triglyceride metabolism remains unknown. In the present study, we found that expression levels of STC2 were significantly reduced in the livers of leptin-deficient and high fat diet-induced obese mice. Systemic administration of STC2 recombinant protein or adenovirus-mediated overexpression of STC2 markedly attenuated hepatosteatosis and hypertriglyceridemia in obese mice. At the molecular level, we found that STC2 activated the STAT3 signaling pathway to inhibit lipogenic gene expression. Consistently, in vitro studies further showed that inhibition of STAT3 signaling abolished the anti-steatotic effects of STC2. Together, our results revealed an important role of STC2 in the regulation of hepatic triglyceride metabolism, which might provide a potential therapeutic target for the treatment of fatty liver and related metabolic disorders

Surface characterization, mechanical properties and corrosion behaviour of ternary based ZneZnOeSiO2composite coating of mild steel

Zinc coatings are obtained either from cyanide, non-cyanide alkaline or acid solutions. Because of the pollution and high cost associated with cyanide, deposition from other baths is gaining importance. In order to develop a bath with additive that could produce a quality coating is the motivation behind this present work which is surface modification of Zne8ZnOeSiO2 nano composite coating on mild steel surface by electrodeposition route. The influence of SiO2 on Zne8ZnO sulphate electrolyte on the properties and microstructure of the produced nano-coatings were investigated. The SiO2 was varied from 0 to 16wt%. The microstructure characteristics of these produced series composites coating were investigated using scanning electron microscopy couple with energy dispersive spectroscopy (SEM/EDS), X-ray diffraction and atomic force microscopy (AFM). The corrosion degradation properties in 3.65% NaCl medium were studied using potentiodynamic polarization technique and characterized by high resolution optical microscope (HR-OPM). The hardness and wear of the composite coating were measured with high diamond microhardness tester and dry abrasive MTR-300 testers respectively. The results showed that average hardness value of 142.5 and 251.2HV and corrosion rate of 0.13088 and 0.00122 mm/yr were obtained for the 0 and 16wt% SiO2 in Zne8ZnO. The work have established that upto 16% SiO2 in Zne8ZnO composite coating on mild steel can be used in improving the microhardness, wear loss and corrosion resistance of mild stee

Elevated Serum Growth Differentiation Factor 15 Levels in Hyperthyroid Patients

Background: Recent studies have shown that growth differentiation factor 15 (GDF15), a member of the transforming growth factor-β (TGF-β)/bone morphogenetic protein (BMP) superfamily, plays an important role in appetite, type 2 diabetes, and cardiovascular diseases. Since thyroid hormone has pleiotropic effects on whole-body energy metabolism, we aimed to explore the effect of thyroid hormone on circulating GDF15 levels in humans and GDF15 genes expression in C57BL/6 mice.Methods: A total of 134 hyperthyroid patients and 105 healthy subjects were recruited. Of them, 43 hyperthyroid patients received thionamide treatment for 3 months until euthyroidism. Serum GDF15 levels were determined using the enzyme-linked immunosorbent assay (ELISA) method. To determine the source for the increased circulating GDF15, C57BL/6 mice were treated with T3, and GDF15 gene expressions in the liver, skeletal muscle, brown adipose tissue (BAT), inguinal white adipose tissue (iWAT), epididymal white adipose tissue (eWAT) were analyzed by quantitative real-time polymerase chain reaction (PCR).Results: Serum GDF15 levels were significantly elevated in hyperthyroid patients as compared with healthy subjects (326.06 ± 124.13 vs. 169.24 ± 82.96 pg/mL; P < 0.001). After thionamide treatment, GDF15 levels in hyperthyroid patients declined markedly from 293.27 ± 119.49 to 118.10 ± 71.83 pg/mL (P < 0.001). After adjustment for potential confounders, serum GDF15 levels were independently associated with hyperthyroidism. T3 treatment increased GDF15 expression in the brown adipose tissue of C57BL/6 mice.Conclusions: Serum GDF15 levels were elevated in patients with hyperthyroidism and declined after thionamide treatment. Thyroid hormone treatment upregulated GDF15 expression in mice. Therefore, our results present the clinical relevance of GDF15 in humans under the condition of hyperthyroidism

The Plant Actin Cytoskeleton Responds to Signals from Microbe-Associated Molecular Patterns

Plants are constantly exposed to a large and diverse array of microbes; however, most plants are immune to the majority of potential invaders and susceptible to only a small subset of pathogens. The cytoskeleton comprises a dynamic intracellular framework that responds rapidly to biotic stresses and supports numerous fundamental cellular processes including vesicle trafficking, endocytosis and the spatial distribution of organelles and protein complexes. For years, the actin cytoskeleton has been assumed to play a role in plant innate immunity against fungi and oomycetes, based largely on static images and pharmacological studies. To date, however, there is little evidence that the host-cell actin cytoskeleton participates in responses to phytopathogenic bacteria. Here, we quantified the spatiotemporal changes in host-cell cytoskeletal architecture during the immune response to pathogenic and non-pathogenic strains of Pseudomonas syringae pv. tomato DC3000. Two distinct changes to host cytoskeletal arrays were observed that correspond to distinct phases of plant-bacterial interactions i.e. the perception of microbe-associated molecular patterns (MAMPs) during pattern-triggered immunity (PTI) and perturbations by effector proteins during effector-triggered susceptibility (ETS). We demonstrate that an immediate increase in actin filament abundance is a conserved and novel component of PTI. Notably, treatment of leaves with a MAMP peptide mimic was sufficient to elicit a rapid change in actin organization in epidermal cells, and this actin response required the host-cell MAMP receptor kinase complex, including FLS2, BAK1 and BIK1. Finally, we found that actin polymerization is necessary for the increase in actin filament density and that blocking this increase with the actin-disrupting drug latrunculin B leads to enhanced susceptibility of host plants to pathogenic and non-pathogenic bacteria