bluuebunny/crossref_metadata_2025_split huggingface dataset:
Growth differentiation factor‐15 (GDF‐15) suppresses in vitro angiogenesis through a novel interaction with connective tissue growth factor (CCN2)
Authors: Whitson Ramon J. , Lucia Marshall Scott , Lambert James R. 
Published: January 2013

AbstractGrowth differentiation factor‐15 (GDF‐15) and the CCN family member, connective tissue growth factor (CCN2), are associated with cardiac disease, inflammation, and cancer. The precise role and signaling mechanism for these factors in normal and diseased tissues remains elusive. Here we demonstrate an interaction between GDF‐15 and CCN2 using yeast two‐hybrid assays and have mapped the domain of interaction to the von Willebrand factor type C domain of CCN2. Biochemical pull down assays using secreted GDF‐15 and His‐tagged CCN2 produced in PC‐3 prostate cancer cells confirmed a direct interaction between these proteins. To investigate the functional consequences of this interaction, in vitro angiogenesis assays were performed. We demonstrate that GDF‐15 blocks CCN2‐mediated tube formation in human umbilical vein endothelial (HUVEC) cells. To examine the molecular mechanism whereby GDF‐15 inhibits CCN2‐mediated angiogenesis, activation of αVβ3 integrins and focal adhesion kinase (FAK) was examined. CCN2‐mediated FAK activation was inhibited by GDF‐15 and was accompanied by a decrease in αVβ3 integrin clustering in HUVEC cells. These results demonstrate, for the first time, a novel signaling pathway for GDF‐15 through interaction with the matricellular signaling molecule CCN2. Furthermore, antagonism of CCN2 mediated angiogenesis by GDF‐15 may provide insight into the functional role of GDF‐15 in disease states. J. Cell. Biochem. 114: 1424–1433, 2013. © 2012 Wiley Periodicals, Inc.
Assessment of density functional methods for reaction energetics: Iridium‐catalyzed water oxidation as case study
Authors: Kazaryan Andranik , Baerends Evert Jan 
Published: January 2013

AbstractWe investigate basis set convergence for a series of density functional theory (DFT) functionals (both hybrid and nonhybrid) and compare to coupled‐cluster with single and double excitations and perturbative triples [CCSD(T)] benchmark calculations. The case studied is the energetics of the water oxidation reaction by an iridium‐oxo complex. Complexation energies for the reactants and products complexes as well as the transition state (TS) energy are considered. Contrary to the expectation of relatively weak basis set dependence for DFT, the basis set effects are large, for example, more than 10 kcal mol−1 difference from converged basis for the activation energy with “small” basis sets (DZ/6‐31G** for Ir/other atoms, or SVP) and still more than 6 kcal mol−1 for def2‐TZVPP/6‐31G**. Inclusion of the dispersion correction in DFT‐D3 schemes affects the energies of reactant complex (RC), TS, and product complex (PC) by almost the same amount; it significantly improves the complexation energy (the formation of RC), but has little effect on the activation energy with respect to RC. With converged basis, some pure GGAs (PBE‐D3, BP86‐D3) as well as the hybrid functional B3LYP‐D3 are very accurate compared to benchmark CCSD(T) calculations. © 2012 Wiley Periodicals, Inc.
Dynamic distribution of HDAC1 and HDAC2 during mitosis: Association with F‐actin
Authors: He Shihua , Khan Dilshad H. , Winter Stefan , Seiser Christian , Davie James R. 
Published: January 2013

AbstractDuring mitosis, histone deacetylase 2 (HDAC2) becomes highly phosphorylated through the action of CK2, and HDAC1 and 2 are displaced from mitotic chromosomes. HDAC1 and 2 are components of corepressor complexes, which function with lysine acetyltransferases to catalyze dynamic protein acetylation and regulate gene expression. In this study, we show that HDAC1 and 2 associate with F‐actin in mitotic cells. Inhibition of Aurora B or protein kinase CK2 did not prevent the displacement of HDAC1 and 2 from mitotic chromosomes in HeLa cells. Further, proteins of the HDAC1 and 2 corepressor complexes and transcription factors recruiting these corepressors to chromatin were dissociated from mitotic chromosomes independent of Aurora B activity. HDAC1 and 2 returned to the nuclei of daughter cells during lamin A/C reassembly and before Sp1, Sp3, and RNA polymerase II. Our results show that HDAC1 and 2 corepressor complexes are removed from the mitotic chromosomes and are available early in the events leading to the re‐establishment of the gene expression program in daughter cells. J. Cell. Physiol. 228: 1525–1535, 2013. © 2012 Wiley Periodicals, Inc.
An integrated understanding of the physiological response to elevated extracellular phosphate
Authors: Camalier Corinne E. , Yi Ming , Yu Li‐Rong , Hood Brian L. , Conrads Kelly A. , Lee Young Jae , Lin Yiming , Garneys Laura M. , Bouloux Gary F. , Young Matthew R. , Veenstra Timothy D. , Stephens Robert M. , Colburn Nancy H. , Conrads Thomas P. , Beck George R. 
Published: January 2013

AbstractRecent studies have suggested that changes in serum phosphate levels influence pathological states associated with aging such as cancer, bone metabolism, and cardiovascular function, even in individuals with normal renal function. The causes are only beginning to be elucidated but are likely a combination of endocrine, paracrine, autocrine, and cell autonomous effects. We have used an integrated quantitative biology approach, combining transcriptomics and proteomics to define a multi‐phase, extracellular phosphate‐induced, signaling network in pre‐osteoblasts as well as primary human and mouse mesenchymal stromal cells. We identified a rapid mitogenic response stimulated by elevated phosphate that results in the induction of immediate early genes including c‐fos. The mechanism of activation requires FGF receptor signaling followed by stimulation of N‐Ras and activation of AP‐1 and serum response elements. A distinct long‐term response also requires FGF receptor signaling and results in N‐Ras activation and expression of genes and secretion of proteins involved in matrix regulation, calcification, and angiogenesis. The late response is synergistically enhanced by addition of FGF23 peptide. The intermediate phase results in increased oxidative phosphorylation and ATP production and is necessary for the late response providing a functional link between the phases. Collectively, the results define elevated phosphate, as a mitogen and define specific mechanisms by which phosphate stimulates proliferation and matrix regulation. Our approach provides a comprehensive understanding of the cellular response to elevated extracellular phosphate, functionally connecting temporally coordinated signaling, transcriptional, and metabolic events with changes in long‐term cell behavior. J. Cell. Physiol. 228: 1536–1550, 2013. © 2012 Wiley Periodicals, Inc.
Glycated collagen and altered glucose increase endothelial cell adhesion strength
Authors: Kemeny Steven Frank , Cicalese Stephanie , Figueroa Dannielle Solomon , Clyne Alisa Morss 
Published: January 2013

AbstractCell adhesion strength is important to cell survival, proliferation, migration, and mechanotransduction, yet changes in endothelial cell adhesion strength have not yet been examined in diseases such as diabetes with high rates of cardiovascular complications. We therefore investigated porcine aortic endothelial cell adhesion strength on native and glycated collagen‐coated substrates and in low, normal, and high glucose culture using a spinning disc apparatus. Adhesion strength increased by 30 dynes/cm2 in cells on glycated collagen as compared to native collagen. Attachment studies revealed that cells use higher adhesion strength αvβ3 integrins to bind to glycated collagen instead of the typical α2β1 integrins used to bind to native collagen. Similarly, endothelial cells cultured in low and high glucose had 15 dynes/cm2 higher adhesion strength than cells in normal glucose after 2 days. Increased adhesion strength was due to elevated VEGF release and intracellular PKC in low and high glucose cells, respectively. Thus glucose increased endothelial cell adhesion strength via different underlying mechanisms. These adhesion strength changes could contribute to diabetic vascular disease, including accelerated atherosclerosis and disordered angiogenesis. J. Cell. Physiol. 228: 1727–1736, 2013. © 2013 Wiley Periodicals, Inc.
Testosterone abrogates TLR4 activation in prostate smooth muscle cells contributing to the preservation of a differentiated phenotype
Authors: Leimgruber Carolina , Quintar Amado Alfredo , García Luciana Noemí , Petiti Juan Pablo , De Paul Ana Lucía , Maldonado Cristina Alicia 
Published: January 2013

AbstractProstate smooth muscle cells (pSMCs) are capable of responding to inflammatory stimuli by secreting proinflammatory products, which causes pSMCs to undergo dedifferentiation. Although it has been proposed that androgens decrease proinflammatory molecules in many cells and under various conditions, the role of testosterone in the prostate inflammatory microenvironment is still unclear. Therefore, our aim was to evaluate if testosterone was able to modulate the pSMCs response to bacterial LPS by stimulating primary pSMC cultures, containing testosterone or vehicle, with LPS (1 or 10 µg/ml) for 24–48 h. The LPS challenge induced pSMCs dedifferentiation as evidenced by a decrease of calponin and alpha smooth muscle actin along with an increase of vimentin in a dose‐dependent manner, whereas testosterone abrogated these alterations. Additionally, an ultrastructural analysis showed that pSMCs acquired a secretory profile after LPS and developed proteinopoietic organelles, while pSMCs preincubated with testosterone maintained a more differentiated phenotype. Testosterone downregulated the expression of surface TLR4 in control cells and inhibited any increase after LPS treatment. Moreover, testosterone prevented IκB‐α degradation and the LPS‐induced NF‐κB nuclear translocation. Testosterone also decreased TNF‐α and IL6 production by pSMCs after LPS as quantified by ELISA. Finally, we observed that testosterone inhibited the induction of pSMCs proliferation incited by LPS. Taken together, these results indicate that testosterone reduced the proinflammatory pSMCs response to LPS, with these cells being less reactive in the presence of androgens. In this context, testosterone might have a homeostatic role by contributing to preserve a contractile phenotype on pSMCs under inflammatory conditions. J. Cell. Physiol. 228: 1551–1560, 2013. © 2012 Wiley Periodicals, Inc.
Analysis of the protein network of cholesterol homeostasis in different brain regions: An age and sex dependent perspective
Authors: Segatto Marco , Di Giovanni Annalaura , Marino Maria , Pallottini Valentina 
Published: January 2013

AbstractAlthough a great knowledge about the patho‐physiological roles of cholesterol metabolism perturbation in several organs has been reached, scarce information is available on the regulation of cholesterol homeostasis in the brain where this lipid is involved in the maintenance of several of neuronal processes. Currently, no study is available in literature dealing how and if sex and age may modulate the major proteins involved in the regulatory network of cholesterol levels in different brain regions. Here, we investigated the behavior of 3‐hydroxy 3‐methylglutaryl coenzyme A reductase (HMGR) and low‐density lipoprotein receptor (LDLr) in adult (3‐month‐old) and aged (12‐month‐old) male and female rats. The analyses were performed in four different brain regions: cortex, brain stem, hippocampus, and cerebellum which represent brain areas characterized by different neuronal cell types, metabolism, cytoarchitecture and white matter composition. The results show that in hippocampus HMGR is lower (30%) in adult female rats than in age‐matched males. Differences in LDLr expression are also observable in old females with respect to age‐matched males: the protein levels increase (40%) in hippocampus and decrease (20%) in cortex, displaying different mechanisms of regulation. The mechanism underlying the observed modifications are ascribable to Insig‐1 and SREBP‐1 modulation. The obtained data demonstrate that age‐ and sex‐related differences in cholesterol homeostasis maintenance exist among brain regions, such as the hippocampus and the prefrontal cortex, important for learning, memory and affection. Some of these differences could be at the root of marked gender disparities observed in clinical disease incidence, manifestation, and prognosis. J. Cell. Physiol. 228: 1561–1567, 2013. © 2012 Wiley Periodicals, Inc.
Pin1 and Nuclear Receptors: A New Language?
Authors: La Montagna Raffaele , Caligiuri Isabella , Giordano Antonio , Rizzolio Flavio 
Published: January 2013

AbstractPin1 is a unique enzyme that can isomerize specific phospho‐Ser/Thr‐Pro peptide bonds, inducing a conformational change in the target protein. Such activity represents a novel and tightly controlled signaling mechanism regulating a spectrum of protein functions during the normal physiology of the cell and in pathological conditions. Our last study demonstrated that Pin1 interacts with the androgen receptor protein and that this interaction is important for its transcriptional activity. Here, we consider the activity that Pin1 plays on the N‐terminal domain of different nuclear receptors and provide an interpretation of this phenomenon. J. Cell. Physiol. 228: 1799–1801, 2013. © 2012 Wiley Periodicals, Inc.
Nck1 deficiency accelerates unloading‐induced bone loss
Authors: Aryal A.C. Smriti , Miyai Kentaro , Hayata Tadayoshi , Notomi Takuya , Nakamoto Tetsuya , Pawson Tony , Ezura Yoichi , Noda Masaki 
Published: January 2013

AbstractMechanical stress is an important signal to determine the levels of bone mass. Unloading‐induced osteoporosis is a critical issue in bed‐ridden patients and astronauts. Many molecules have been suggested to be involved in sensing mechanical stress in bone, though the mechanisms involved in this phenomenon are not fully understood. Nck1 is an adaptor protein known to mediate signaling from plasma membrane‐activated receptors to cytosolic effectors regulating actin cytoskeleton remodeling. Nck1 has also been implicated in cellular responses to endoplasmic reticulum stress. In vitro, in case of cell stress the actin cytoskeleton is disrupted and in such cases Nck1 has been reported to enter the nucleus of the cells to mediate the nuclear actin polymerization. However, the role of Nck1 in vivo during the bone response to mechanical stimuli is unknown. The purpose of this study is to examine the role of Nck1 in unloading‐induced bone loss in vivo. Sciatic and femoral nerve resection was conducted. Neurectomy‐based unloading enhanced Nck1 gene expression in bone about twofold. Using the Nck1 deficient mice and control Nck1+/+, effects of neurectomy‐based unloading on bone structure were examined. Unloading reduced bone volume in wild type mice by 30% whereas the levels in bone loss were exacerbated to 50% in Nck1 deficient mice due to neurectomy after 4 weeks. These data demonstrate that Nck1 gene deficiency accelerates the mechanical unloading‐induced bone loss suggesting Nck1 to be a crucial molecule in mechanical stress mediated regulation in bone metabolism. J. Cell. Physiol. 228: 1397–1403, 2013. © 2012 Wiley Periodicals, Inc.
Galectin‐3 deficiency protects pancreatic islet cells from cytokine‐triggered apoptosis in vitro
Authors: Saksida Tamara , Nikolic Ivana , Vujicic Milica , Nilsson Ulf J. , Leffler Hakon , Lukic Miodrag L. , Stojanovic Ivana , Stosic‐Grujicic Stanislava 
Published: January 2013

AbstractBeta cell apoptosis is a hallmark of diabetes. Since we have previously shown that galectin‐3 deficient (LGALS3−/−) mice are relatively resistant to diabetes induction, the aim of this study was to examine whether beta cell apoptosis depends on the presence of galectin‐3 and to delineate the underlying mechanism. Deficiency of galectin‐3, either hereditary or induced through application of chemical inhibitors, β‐lactose or TD139, supported survival and function of islet beta cells compromised by TNF‐α + IFN‐γ + IL‐1β stimulus. Similarly, inhibition of galectin‐3 by β‐lactose or TD139 reduced cytokine‐triggered apoptosis of beta cells, leading to conclusion that endogenous galectin‐3 propagates beta apoptosis in the presence of an inflammatory milieu. Exploring apoptosis‐related molecules expression in primary islet cells before and after treatment with cytokines we found that galectin‐3 ablation affected the expression of major components of mitochondrial apoptotic pathway, such as BAX, caspase‐9, Apaf, SMAC, caspase‐3, and AIF. In contrast, anti‐apoptotic molecules Bcl‐2 and Bcl‐XL were up‐regulated in LGALS3−/− islet cells when compared to wild‐type (WT) counterparts (C57BL/6), resulting in increased ratio of anti‐apoptotic versus pro‐apoptotic molecules. However, Fas‐triggered apoptotic pathway as well as extracellular signal‐regulated kinase 1/2 (ERK1/2) was not influenced by LGALS‐3 deletion. All together, these results point to an important role of endogenous galectin‐3 in beta cell apoptosis in the inflammatory milieu that occurs during diabetes pathogenesis and implicates impairment of mitochondrial apoptotic pathway as a key event in protection from beta cell apoptosis in the absence of galectin‐3. J. Cell. Physiol. 228: 1568–1576, 2013. © 2012 Wiley Periodicals, Inc.
Comparison of control strategies for fed‐batch culture of hybridoma cells based on on‐line monitoring of oxygen uptake rate, optical cell density and glucose concentration
Authors: Casablancas Antoni , Gámez Xavier , Lecina Martí , Solà Carles , Cairó Jordi J. , Gòdia Francesc 
Published: January 2013

AbstractBACKGROUNDImprovement of the mammalian cell culture process is based on the implementation of culture strategies with higher productivities, such as fed‐batch or perfusion processes. The efficient development of these culture strategies depends strongly on the availability of suitable monitoring tools to determine the activity of cell culture and adjust nutrient feeding correspondingly.RESULTSIn this study oxygen uptake rate (OUR), cell density and glucose concentration on‐line monitoring systems are applied to control fed‐batch processes. Different combinations of these monitoring systems were used to determine cell growth and metabolic activity of cell culture in order to adjust substrate feeding in a balanced manner. Application of these monitoring tools in fed‐batch processes allowed extension of the exponential growth of hybridoma cells up to 2–3‐fold and increased antibody productivity from 84 to 168% with respect to conventional batch culture.CONCLUSIONSThe three control strategies tested have been successful in providing improvement of the fed‐batch culture of the hybridoma cell line used. Among the different alternatives studied, the use of OUR on‐line monitoring to simultaneously determine cell growth and metabolic activity appears to be the best method to adjust substrate feeding owing to its simplicity and robustness. © 2012 Society of Chemical Industry
Bioremediation of nitrate‐polluted groundwater in a microbial fuel cell
Authors: Pous Narcis , Puig Sebastià , Coma Marta , Balaguer Maria D. , Colprim Jesus 
Published: January 2013

AbstractBACKGROUNDGroundwater quality is threatened by nitrate accumulation in several regions around the world. Nitrate must be removed from contaminated groundwater to use it as drinking water. Microbial fuel cells (MFCs) can be used for autotrophic denitrification. Thus, the use of MFCs is a potential alternative to using traditional methods for treating nitrate‐polluted groundwater.RESULTSThe objective of this study was to evaluate the potential of MFC technology to treat nitrate‐polluted groundwater (28.32 ± 6.15 mgN‐NO3− L−1). The bioanode was fed with an acetate solution that permitted electron and proton flux to the biocathode. Initially, nitrite was observed in the effluent. After 97 days of operation, the denitrifying‐MFC reduced the nitrate and nitrite concentrations in the effluent (12.14 ± 3.59 mgN‐NO3− L−1 and 0.14 ± 0.13 mgN‐NO2− L−1).Thus, this method improved water quality to meet World Health Organisation standards. However, nitrous oxide emissions were deduced from the electron balance, cathode coulumbic efficiency and Tafel plots. Bioelectrochemical evolution of the biocathode was related to the denitrification nature (sequential reaction steps from NO3− to N2, through NO2− and N2O as stable intermediates) and was supported by the Tafel plots.CONCLUSIONThe bioremediation of nitrate‐polluted groundwater with a MFC biocathode is feasible. © 2012 Society of Chemical Industry
Evaluation of UV/H2O2 for the disinfection and treatment of municipal secondary effluents for water reuse
Authors: Souza Bruno S. , Dantas Renato F. , Agulló‐Barceló Míriam , Lucena Francisco , Sans Carme , Esplugas Santiago , Dezotti Márcia 
Published: January 2013

AbstractBACKGROUNDIn this work, photochemical treatment (UV/H2O2) of a municipal secondary effluent was studied to assess its suitability for preparing water for reuse. Ten water reuse criteria obtained from the legislation of eight countries were used as indicators of water quality. Effluents from the municipal wastewater treatment plant (WWTP) of Gavà‐Viladecans (Barcelona, Spain) were subjected to UV/H2O2 treatment with low H2O2 concentration ([H2O2]o = 5 mg L−1 and UV fluence = 8.04 mW cm−2) and the most common water reuse parameters, such as disinfection indicators, turbidity, total suspended solids and microcontaminant removal (atrazine), were monitored.RESULTSTreatment inactivated 100% of the disinfection indicators after 5 min. Afterwards, three levels of treatment corresponding to different reuse applications were defined according to the legislation used. In addition, according to the LuminoTox® bioassay, oxidative treatment of the secondary effluent favoured the formation of less toxic intermediates. Finally, a study was performed to determine the costs of each reuse condition.CONCLUSIONSFindings suggest that UV/H2O2 is a suitable method to obtain water of sufficient quality for further reuse. © 2012 Society of Chemical Industry
Defluoridation from aqueous solution by chitosan modified natural zeolite
Authors: Peng Sha , Zeng Qinghui , Guo Yucheng , Niu Beibei , Zhang Xu , Hong Song 
Published: January 2013

AbstractBACKGROUNDA novel hybrid material, chitosan‐modified zeolite (Ch‐Z), was synthesized for defluoridation. The structure was characterized by Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), X‐ray diffraction (XRD) and thermogravimetric analysis (TGA).RESULTSThe maximum defluoridation capacity onto Ch‐Z was 4.16 mg g−1 from an initial fluoride concentration of 40 mg L‐1, which was almost three times higher than that of unmodified zeolite. The adsorption kinetics of fluoride onto Ch‐Z and zeolite followed pseudo‐second‐order and intra‐particle diffusion models, respectively. Based on a nonlinear method, the adsorption of fluoride onto Ch‐Z fitted the Freundlich and Redlich–Peterson isotherm models well. Various physicochemical parameters affecting the adsorption of fluoride onto Ch‐Z were investigated. It was observed that the maximum uptake of fluoride occurred in a pH range 4.5–5.5.CONCLUSIONAlthough among various ions the presence of high concentration carbonate ions in aqueous solution had the greatest adverse impact on the adsorption of fluoride, Ch‐Z can be successfully used for treatment of real water samples. © 2012 Society of Chemical Industry