bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of nuclear factor‐κB in rats of radiocontrast‐media‐induced nephropathy
Authors: Xu XunHui , Wu TianHua , Ding XiaoQiang , Zhu JiaMing , Zou JianZhou , He JianQiang 
Published: December 2008

AbstractThis study was undertaken to examine the possible role of the DNA‐binding activity of nuclear factor‐kappa B (NF‐κB) in rat of radiocontrast‐media‐induced nephropathy (RCIN) and to explore the characteristic of RCIN in rats and the role of NF‐κB in its occurrence. Forty‐eight adult male Sprague–Dawley (SD) rats were randomly divided into Groups A–D. Rats of Groups A and B were intravenously injected with NG‐nitro‐L‐arginine methyl ester (L‐NAME) (10 mg/kg) and indomethacin (10 mg/kg), respectively. Rats of Groups C and D were intravenously injected with 1‐M phosphate buffer (PH = 8.4 3 mL/kg) and normal saline (NS 2 mL/kg), respectively. After 30 min, Groups A and D were injected with NS (8 mL/kg) and Groups B and C were injected with diatrizoate (DTZ 8 mL/kg). After injected contrast media (CM) for 6 h, the serum creatinine and blood urea nitrogen of rat in Group B increased sharply as compared with Groups A, C, and D. After 48 h, the data recovered to 49.28 ± 8.81 μmol/L and 6.72 ± 2.75 mmol/L, respectively. Vacuolization of the tubule epithelial cells of the kidney was observed in Group A. Especially, these pathological changes were most obvious in outer medulla. Contrast to group A, the DNA‐binding activity of NF‐κB in rat kidney of Group B reached a peak at the 6th h and recovered to the normal level after the 48th h. CM mainly damages renal tubular–interstitial, which appears the earliest and most serious in the outer medulla. Activation of NF‐κB of renal may be one of the mechanisms of RCIN occurrence. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:416–421, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20256
HDAC4 contributes to IL‐1‐induced mPGES‐1 expression in human synovial fibroblasts through up‐regulation of Egr‐1 transcriptional activity
Authors: Chabane Nadir , Li Xinfang , Fahmi Hassan 
Published: December 2008

AbstractMicrosomal prostaglandin E synthase‐1 (mPGES‐1) catalyzes the terminal step in the biosynthesis of PGE2, which contributes to many physiopathological processes. We show here that inhibitors of histone deacetylase (HDAC) activity, trichostatin A (TSA), butyric acid (BA), and valproic acid (BA) prevented IL‐1‐induced mPGES‐1 protein expression in human synovial fibroblasts. TSA also inhibited IL‐1‐induced mPGES‐1 mRNA expression and promoter activation. Overexpression of HDAC4, but not of HDAC1, 2, 3, 5, or 6 enhanced, whereas HDAC4 silencing with small interfering RNA (siRNA) reduced, IL‐1‐induced mPGES‐1 promoter activation, implying that HDAC4 contributes to mPGES‐1 gene expression. Consistently, IL‐1‐induced mPGES‐1 protein expression was prevented by siRNA for HDAC4. We also demonstrate that IL‐1‐induced HDAC4 recruitment to the mPGES‐1 promoter. This recruitment was not accompanied by deacetylation of histones H3 and H4, suggesting that HDAC4 contributes to mPGES‐1 induction independently of local deacetylation of histones H3 and H4. We then investigated whether HDAC4 regulates mPGES‐1 expression by modulating the activity of Egr‐1, a key transcription factor in IL‐1‐induced mPGES‐1 expression. We found that HDAC4 overexpression enhances, whereas HDAC4 knockdown by siRNA reduces Egr‐1‐mediated activation of the mPGES‐1 promoter. Together these data indicate that HDAC4 contributes to transcriptional induction of mPGES‐1 by IL‐1 through a mechanism involving up‐regulation of Egr‐1 transcriptional activity. J. Cell. Biochem. 106: 453–463, 2009. © 2008 Wiley‐Liss, Inc.
Effect of tamoxifen and retinoic acid on bradykinin induced proliferation in MCF‐7 cells
Authors: Searovic Paola , Alonso Marcelo , Oses Carolina , Pereira‐Flores Karla , Velarde Victoria , Saez Claudia G. 
Published: December 2008

AbstractChemopreventive approaches for the treatment of breast cancer have been validated clinically and with in vitro studies. The combined action of tamoxifen/all‐trans retinoic acid was advantageous in MCF‐7 cells, reducing cell proliferation, Bcl‐2 and c‐Myc protein levels and increasing E‐Cadherin protein levels and Gap junctional Intercellular Communication. We further investigated their combined effect in the presence of bradykinin, a pro‐inflammatory agent, previously reported to contribute to the proliferation of breast cancer cells. Bradykinin increased MCF‐7 cell proliferation, c‐Myc levels and ERK1/2 activity. The co‐incubation of bradykinin‐MCF‐7 cells with tamoxifen/all‐trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl‐2, c‐Myc, and bradykinin receptor‐2 levels, without altering the enhanced E‐cadherin levels induced by tamoxifen/all‐trans retinoic acid. We showed that the anti‐tumoral effect of tamoxifen/all‐trans retinoic acid is beneficial in MCF‐7 breast cancer cells grown in a bradykinin‐pro‐mitogenic environment, an effect that might be, at least in part, through the MAPK pathway and B2‐bradykinin receptor inhibition. J. Cell. Biochem. 106: 473–481, 2009. © 2008 Wiley‐Liss, Inc.
8‐chloro‐adenosine‐induced E2F1 promotes p14ARF gene activation in H1299 cells through displacing Sp1 from multiple overlapping E2F1/Sp1 sites
Authors: Zhang Hai‐Jun , Li Wen‐Juan , Yang Sheng‐Yong , Li Shu‐Yan , Ni Ju‐Hua , Jia Hong‐Ti 
Published: December 2008

AbstractThe regulation of p14ARF gene by E2F transcription factor, which differs from that of classical E2F targets, has recently been attributed to a variant E2F‐response element. However, promoter assays suggest multiple elements present in the p14ARF promoter and argue against the idea that the ARF promoter has a unique ability to distinguish between aberrant and physiological levels of E2F1. Therefore, the functional characterization of the promoter still needs to be done. We demonstrate that at least two overlapping E2F1/Sp1 binding sites are present in the p14ARF promoter, and E2F1 activates the promoter through displacing constitutive Sp1 from the overlapping sites. We found that 8‐chloro‐adenosine (a metabolite of 8‐Cl‐cAMP) exposure induced the p14ARF gene in human lung cancer H1299 cells, followed by increased expression of E2F1 and constitutive expression of Sp1. The combination of cotransfection and electrophoretic mobility shift assay (EMSA) indicated that constitutive binding of Sp1 to the overlapping sites contributed to a constitutive expression of the ARF gene in unexposed H1299, whereas displacing Sp1 from the overlapping sites by E2F1 promoted the gene activation after exposure. EMSA and chromatin immunoprecipitation revealed increased association of E2F1 with the overlapping sites in the active promoter in 8‐Cl‐Ado‐exposed cells. Together, these data suggest that the overlapping E2F1/Sp1 site, being present in multiple copies in the p14ARF promoter, may serve as the targets for both E2F1 and Sp1, thereby playing a crucial role in response to some oncogenic signals and stimulators, which activate the ARF gene through inducing E2F in the cell. J. Cell. Biochem. 106: 464–472, 2009. © 2008 Wiley‐Liss, Inc.
Loss of profilin‐1 expression enhances breast cancer cell motility by Ena/VASP proteins
Authors: Bae Yong Ho , Ding Zhijie , Zou Li , Wells Alan , Gertler Frank , Roy Partha 
Published: December 2008

AbstractWe previously showed that silencing profilin‐1 (Pfn1) expression increases breast cancer cell motility, but the underlying mechanisms have not been explored. Herein, we demonstrate that loss of Pfn1 expression leads to slower but more stable lamellipodial protrusion thereby enhancing the net protrusion rate and the overall motility of MDA‐MB‐231 breast cancer cells. Interestingly, MDA‐MB‐231 cells showed dramatic enrichment of VASP at their leading edge when Pfn1 expression was downregulated and this observation was also reproducible in other cell types including human mammary epithelial cells and vascular endothelial cells. We further demonstrate that Pfn1 downregulation results in a hyper‐motile phenotype of MDA‐MB‐231 cells in an Ena/VASP‐dependent mechanism. Pfn1‐depleted cells display a strong colocalization of VASP with lamellipodin (Lpd—a PI(3,4)P2‐binding protein that has been previously implicated in lamellipodial targeting of Ena/VASP) at the leading edge. Finally, inhibition of PI3‐kinase (important for generation of PI(3,4)P2) delocalizes VASP from the leading edge. This observation is consistent with a possible involvement of Lpd in enhanced membrane recruitment of VASP that results from loss of Pfn1 expression. Our findings for the first time highlight a possible mechanism of how reduced expression of a pro‐migratory molecule like Pfn1 could actually promote motility of breast cancer cells. J. Cell. Physiol. 219: 354–364, 2009. © 2008 Wiley‐Liss, Inc.
Over‐expression of glycerol dehydrogenase and 1,3‐propanediol oxidoreductase in Klebsiella pneumoniae and their effects on conversion of glycerol into 1,3‐propanediol in resting cell system
Authors: Zhao Li , Ma Xingyuan , Zheng Yu , Zhang Jianguo , Wei Guodong , Wei Dongzhi 
Published: December 2008

AbstractBACKGROUND: Glycerol dehydrogenase [EC.1.1.1.6] and 1,3‐propanediol oxidoreductase [EC.1.1.1.202] were proved to be two of the key enzymes for glycerol conversion to 1,3‐propanediol in Klebsiella pneumoniae under anaerobic conditions. For insight into their significance on 1,3‐propanediol production under micro‐aerobic conditions, these two enzymes were over‐expressed in K. pneumoniae individually, and their effects on conversion of glycerol into 1,3‐propanediol in a resting cell system under micro‐aerobic conditions were investigated.RESULTS: In the resting cell system, over‐expression of 1,3‐propanediol oxidoreductase led to faster glycerol conversion and 1,3‐propanediol production. After a 12 h conversion process, it improved the yield of 1,3‐propanediol by 20.4% (222.1 mmol L−1 versus 184.4 mmol L−1) and enhanced the conversion ratio of glycerol into 1,3‐propanediol from 50.8% to 59.8% (mol mol−1). Over‐expression of glycerol dehydrogenase in K. pneumoniae had no significant influence both on 1,3‐propanediol yield and on the conversion ratio of glycerol into 1,3‐propanediol in the resting cell system.CONCLUSION: The results were important for an understanding of the significance of glycerol dehydrogenase and 1,3‐propanediol oxidoreductase in 1,3‐proanediol production under micro‐aerobic conditions, and for developing better strategies to improve 1,3‐propanediol yield. Copyright © 2008 Society of Chemical Industry
Supercritical CO2 extraction of pigment components with pharmaceutical importance from Chlorella vulgaris
Authors: Kitada Kiwa , Machmudah Siti , Sasaki Mitsuru , Goto Motonobu , Nakashima Yuya , Kumamoto Shoichiro , Hasegawa Takashi 
Published: December 2008

AbstractBACKGROUND: Chlorella vulgaris is a green microalgae that contains various pigment components of carotenoids and chlorophylls. Supercritical CO2 is widely used for extraction of pharmaceutical compounds because it is non‐oxic and easily separated from extracted material by simply depressurizing. In this work, pharmaceutical compounds from Chlorella vulgaris have been extracted using supercritical CO2 with or without entrainer at various extraction conditions.RESULTS: Based on high performance liquid chromatography (HPLC) analysis, the extracts contained pigment components, such as lutein, β‐carotene, chlorophyll a and b. Higher extraction pressure and temperature promoted higher lutein extraction by supercritical CO2. The optimum pressure and temperature for extraction were obtained as 50 MPa and 80 °C. Ethanol as an entrainer was more effective than acetone for the extraction of pigment components. Pigment components in the extract obtained by supercritical CO2 with and without entrainer were compared with the extract obtained by a conventional extraction method.CONCLUSION: Supercritical CO2 has been successfully applied for the extraction of pigment components from Chlorella vulgaris. Supercritical CO2 enabled high selectivity for lutein extraction; however, the lutein yield was lower than that obtained by extraction using supercritical CO2 with ethanol and soxhlet. Copyright © 2008 Society of Chemical Industry
Green tissue‐specific production of a microbial endo‐cellulase in maize (Zea mays L.) endoplasmic‐reticulum and mitochondria converts cellulose into fermentable sugars
Authors: Mei Chuansheng , Park Sang‐Hyuck , Sabzikar Robab , Callista Ransom Chunfang Qi , Sticklen Mariam 
Published: December 2008

AbstractBACKGROUND: Commercial conversion of lignocellulosic biomass to fermentable sugars for biofuels and chemical byproducts uses relatively expensive bulk production of biologically active cellulase enzymes, which could alternatively be achieved by using solar energy for direct production of these enzymes within feedstock crop cellulosic biomass.RESULTS: The Acidothermus cellulolyticus endo‐cellulase E1 has been produced in transgenic maize plants. This heterologous enzyme was specifically targeted for accumulation into two sub‐cellular compartments, endoplasmic reticulum (ER) or mitochondria of plant leaves and stalks. Furthermore, successful use of this maize‐produced heterologous cellulase in converting cellulose into fermentable sugars for biofuels, has been confirmed.CONCLUSIONS: Green‐specific expression of cellulases in maize plants can avoid public controversies associated with production of transgene products in maize seeds and/or pollen. Sub‐cellular targeting of cellulases may result in better expression of transgene products because these compartments, specially ER, normally contain molecular chaperones that enhance protein folding and there the biological activity. Also, using solar energy to produce cellulases within crop cellulosic biomass can replace the costly process of cellulase production in microbial bioreactors, and therefore, save costs. Copyright © 2008 Society of Chemical Industry
Cobalt removal from waste‐water by means of supported liquid membranes
Authors: Verbeken Kim , Vanheule Bruno , Pinoy Luc , Verhaege Marc 
Published: December 2008

AbstractBACKGROUND: Supported liquid membranes (SLM) are an alternative technique to remove and recover metals from diluted process solutions and waste‐water. In the present work, the removal of Co(II) from a synthetic CoSO4 solution containing initial amounts of cobalt(II) in the range 100–200 ppm (0.1–0.2 g dm−3) has been studied on a pilot scale. By performing batch equilibrium experiments, the optimal settings, i.e. the composition of the organic phase, the pH of the feed, the type and concentration of the stripping agent were determined.RESULTS: It is shown that the equilibrium characteristics of a synergistic extractant mixture containing di‐2‐ethyl‐hexylphosphoric acid (D2EHPA) and 5‐dodecylsalicylaldoxime (LIX 860‐I) are superior to D2EHPA. Both hydrochloric acid and sulfuric acid have been evaluated as stripping solutions in liquid–liquid extraction tests and as the receiving phase in a SLM configuration. Although equilibrium tests showed no difference in stripping characteristics between both chemicals, it was observed that in a SLM configuration the stability of the system when hydrochloric acid is used is poor. With a commercially available SLM module (Liqui‐Cel Extra‐Flow 4 × 28) having a surface area of 19 m2, a steady Co(II) flux of 0.140 gm−2h−1 has been obtained at influent concentrations of cobalt between 100 and 200 ppm with 3 mol dm−3 sulfuric acid as stripping phase.CONCLUSIONS: The results obtained show that a supported liquid membrane containing a synergistic mixture of LIX 860‐I and D2EHPA gives the possibility of recovering cobalt from dilute solutions. Copyright © 2008 Society of Chemical Industry
Analysis of mice with targeted deletion of AQP9 gene provides conclusive evidence for expression of AQP9 in neurons
Authors: Mylonakou Maria N. , Petersen Petur H. , Rinvik Eric , Rojek Aleksandra , Valdimarsdottir Erla , Zelenin Sergey , Zeuthen Thomas , Nielsen Søren , Ottersen Ole P. , Amiry‐Moghaddam Mahmood 
Published: December 2008

AbstractAQP9 is an aquaglyceroporin that serves important functions in peripheral organs, including the liver. Reflecting the lack of AQP9 knockout mice, uncertainties still prevail regarding the localization and roles of AQP9 in the central nervous system. Here we present a comprehensive analysis of AQP9 gene expression in brain, based on a quantitative and multipronged approach that includes the use of animals with targeted deletion of the AQP9 gene. We show by real‐time PCR that AQP9 mRNA concentration in rat and mouse brain is ∼3% and ∼0.5%, respectively, of that in rat and mouse liver, the organ with the highest level of AQP9. By blue native gel analysis it could be demonstrated that the brain contains tetrameric AQP9, corresponding to the functional form of AQP9. The band corresponding to the AQP9 tetramer was absent in AQP9 knockout brain and liver. Immunocytochemistry and in situ hybridization analyses with AQP9 knockout controls show that subpopulations of nigral neurons express AQP9 both at the mRNA and at the protein levels and that populations of cortical cells (including hilar neurons in the hippocampus) contain AQP9 mRNA but no detectable AQP9 immunosignal. The present data provide conclusive evidence for the presence of tetrameric AQP9 in brain and for the expression of AQP9 in neurons. © 2008 Wiley‐Liss, Inc.
AUF1 and Hu proteins in the developing rat brain: Implication in the proliferation and differentiation of neural progenitors
Authors: Hambardzumyan Dolores , Sergent‐Tanguy Solène , Thinard Reynald , Bonnamain Virginie , Masip Manuel , Fabre Annabelle , Boudin Hélène , Neveu Isabelle , Naveilhan Philippe 
Published: December 2008

AbstractPosttranscriptional events such as RNA stabilization are important for cell differentiation, but little is known about the impact of AU‐rich binding proteins (AUBPs) on the fate of neural cells. Expression of destabilizing AUBPs such as AUF1 and neuronal‐specific stabilizing proteins such as HuB, HuC and HuD was therefore analyzed in the developing central nervous system. Real‐time RT‐PCR indicated a specific developmental pattern in the postnatal cerebellum, with a progressive down‐regulation of AUF1 from P1, whereas HuB was strongly up‐regulated at about P7. These changes were accompanied by a progressive increase in AUF1p45 and the disappearance of one HuB isoform from P15, suggesting particular roles for these AUBPs in the developing cerebellum. AUF1 was detected in the three main cerebellar layers, whereas Hu proteins were found only in postmitotic neurons. A role for Hu proteins in the early stages of neuronal differentiation is further supported by arrest of cell proliferation following induction of HuB or HuD expression in a neural stem cell line. The decrease in nestin expression suggest that HuD, but not HuB, favors the transition of neural progenitors into early neuroblasts, but other factors are most probably required for their full differentiation into neurons, insofar as GAP‐43 was not detected in HuD‐transfected cells. These data suggest critical roles for HuB at the very earliest stages of neuronal differentiation, such as cell cycle exit, and HuD might also be involved in the transition of neural progenitors into early neuroblasts. Taken together, the present results strengthen the importance of AUBPs in brain ontogenesis. © 2008 Wiley‐Liss, Inc.
Aberrant axonal projections from mammillary bodies in Pax6 mutant mice: Possible roles of Netrin‐1 and Slit 2 in mammillary projections
Authors: Tsuchiya Reiko , Takahashi Kaoru , Liu Fu‐Chin , Takahashi Hiroshi 
Published: December 2008

AbstractEarly events in the axonal tract formation from mammillary bodies remain poorly understood. In the present study, we reported an aberrant pattern of axonal projections from mammillary bodies to the dorsal thalamus in mice lacking the transcription factor Pax6. We found that Netrin‐1 was ectopically up‐regulated and that both Slit1 and Slit2 were down‐regulated in the presumptive dorsal thalamus of Pax6 mutant mice. We then examined the effects of Netrin‐1 and Slit2 on the mammillary axons by in utero electroporation techniques. Netrin‐1 had an attractive action toward the mammillary axons. Moreover, mammillary trajectories were disorganized in Netrin‐1‐deficient mice. On the other hand, Slit2 had a repulsive effect on the mammillary axons. These findings suggest that the combination of Netrin and Slit may be involved in proper axonal projection from the mammillary bodies and that their misexpression in the diencephalon may cause the misrouting of these axons in Pax6 mutant mice. © 2008 Wiley‐Liss, Inc.
Neuroanatomical relationships of substance P‐immunoreactive intrapulmonary C‐fibers and nicotinic cholinergic receptors
Authors: Dehkordi Ozra , Rose Jed E. , Balan Kannan V. , Kc Prabha , Millis Richard M. , Jayam‐Trouth Annapurni 
Published: December 2008

AbstractPrevious studies have suggested that sensory mechanisms may be important components of addiction to, and withdrawal from, cigarette smoking. The sensory and respiratory responses to nicotine are mediated, in part, by bronchopulmonary C‐fiber afferents. Nicotine has a direct stimulatory effect on pulmonary sensory neurons, and nicotinic cholinergic receptors (nAChRs) composed of various combinations of α and β subunits are known to be present in pulmonary ganglia. At the subcellular level, however, little is known about expression of nAChRs on sensory fibers in the intrapulmonary airways. The present study was therefore designed to evaluate the expression of nAChRs on a subset of intrapulmonary sensory nerve endings known to exhibit immunoreactivity for substance P (SP). The presence of nAChR subunits was first confirmed at the mRNA and protein levels in rat lung tissues by using RT‐PCR and Western blot techniques. Then, double labeling of SP‐immunoreactive (‐IR) C‐fibers and different nAChR subunits was performed. α2, α3, α4, α5, α7, and β2 subunits were detected at all levels of the intrapulmonary airways; including bronchi, terminal and respiratory bronchioles, alveolar walls, and alveolar macrophages. None of the nAChR subunits studied was expressed by the SP‐IR C‐fibers. However, SP‐expressing C‐fibers were observed in close proximity to and intermingling with nAChR‐expressing airway epithelial cells. The close proximity of C‐fibers to nAChR‐expressing airway epithelial cells suggests that a component of nicotinic stimulation of SP‐IR C‐fiber afferents may be mediated by endogenous chemical substances released by nAChR‐expressing epithelial cells. © 2008 Wiley‐Liss, Inc.