bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of AP1 element in the activation of human eNOS promoter by lysophosphatidycholine
Authors: Xing Feiyue , Jiang Yong , Liu Jing , Zhao Kesen , Mo Yongyan , Qin Qinghe , Wang Jingzhen , Ouyang Jianming , Zeng Yaoying 
Published: February 2006

AbstractHuman endothelial nitric oxide synthase (eNOS) plays a crucial role in maintaining blood pressure homeostasis and vascular integrity. It, therefore, is very essential to elucidate the regulation of it. In the current study, a red fluorescent protein (RFP) reporter system containing human eNOS promoter was first constructed, being characteristics of real time morphologic and quantitative analysis for the same sample. It was observed by DNA sequence deletion that 68% of the basal activity of the promoter was controlled by the region from −1 to −166 bp, and 32% of it was dependent on the region from −1,033 to −1,600 bp. The mutation of SSRE element (−999∼−994 bp) and wild‐type SSRE decoy oligodeoxynucleotides (ODN) did not alter the basal activity and the stimulating activity by lysophosphatidycholine (LPC). The mutation of upstream AP1 element (−1,530∼−1,524 bp) did not affect the basal activity, but resulted in near 30% reduction in the stimulating activity by LPC. Moreover, wild‐type AP1 decoy ODN also remarkably attenuated it. It was proved by EMSA analysis that LPC indeed enhanced the activity of AP1 transcriptional factor binding to AP1 element. However, the role of AP1 was dependent on the presence of SP1, which was proved by the combining mutation of AP1 with SP1. The mutation of downstream AP1 element (−662∼−656 bp) had no influence on the basal and stimulating activities by LPC. These results strongly suggest that the main functional region of the promoter is from −1 bp to −166 bp, that the upstream AP1 participates in the activation of the promoter by LPC on the premise of the presence of SP1, and that the downstream AP1 and SSRE do not involve the basal and stimulating activity by LPC. J. Cell. Biochem. 98: 872–884, 2006. © 2006 Wiley‐Liss, Inc.
Expression of DNMT3A transcripts and nucleolar localization of DNMT3A protein in human testicular and fibroblast cells suggest a role for de novo DNA methylation in nucleolar inactivation
Authors: Galetzka Danuta , Tralau Tim , Stein Raimund , Haaf Thomas 
Published: February 2006

AbstractTranscriptional silencing during differentiation of human male germ cells and serum starvation of human fibroblasts is controlled by epigenetic mechanisms that involve de novo DNA methylation. It is associated with high expression of different trancripts of the DNA methyltransferase 3A (DNMT3A) gene that encode two isoforms with de novo methyltransferase activity and one without catalytic activity. Western blots revealed that DNMT3A protein (with catalytic domain) is present at low levels in several tissues and at increased levels in testicular cells and growth‐arrested fibroblasts. Immunofluorescence experiments localized DNMT3A to discrete nucleolar foci in B spermatogonia and resting fibroblasts. The data here suggest a role for de novo DNA methylation in nucleolar inactivation. J. Cell. Biochem. 98: 885–894, 2006. © 2006 Wiley‐Liss, Inc.
Functional and structural properties of stannin: Roles in cellular growth, selective toxicity, and mitochondrial responses to injury
Authors: Billingsley M.L. , Yun J. , Reese B.E. , Davidson C.E. , Buck‐Koehntop B.A. , Veglia G. 
Published: February 2006

AbstractStannin (Snn) was discovered using subtractive hybridization methodology designed to find gene products related to selective organotin toxicity and apoptosis. The cDNAs for Snn were first isolated from brain tissues sensitive to trimethyltin, and were subsequently used to localize, characterize, and identify genomic DNA, and other gene products of Snn. Snn is a highly conserved, 88 amino acid protein found primarily in vertebrates. There is a minor divergence in the C‐terminal sequence between amphibians and primates, but a nearly complete conservation of the first 60 residues in all vertebrates sequenced to date. Snn is a membrane‐bound protein and is localized, in part, to the mitochondria and other vesicular organelles, suggesting that both localization and conservation are significant for the overall function of the protein. The structure of Snn in a micellar environment and its architecture in lipid bilayers have been determined using a combination of solution and solid‐state NMR, respectively. Snn structure comprised a single transmembrane domain (residues 10–33), a 28‐residue linker region from residues 34–60 that contains a conserved CXC metal binding motif and a putative 14‐3‐3ξ binding region, and a cytoplasmic helix (residues 61–79), which is partially embedded into the membrane. Of primary interest is understanding how this highly‐conserved peptide with an interesting structure and cellular localization transmits both normal and potentially toxic signals within the cell. Evidence to date suggests that organotins such as trimethyltin interact with the CXC region of Snn, which is vicinal to the putative 14‐3‐3 binding site. In vitro transfection analyses and microarray experiments have inferred a possible role of Snn in several key signaling systems, including activation of the p38‐ERK cascade, p53‐dependent pathways, and 14‐3‐3ξ protein‐mediated processes. TNFα can induce Snn mRNA expression in endothelial cells in a PKC‐ε dependent manner. Studies with Snn siRNA suggest that this protein may be involved in growth regulation, since inhibition of Snn expression alone leads to reduced endothelial cells growth and induction of COP‐1, a negative regulator of p53 function. A key piece of the puzzle, however, is how and why such a highly‐conserved protein, localized to mitochondria, interacts with other regulatory proteins to alter growth and apoptosis. By knowing the structure, location, and possible signaling pathways involved, we propose that Snn constitutes an important sensor of mitochondrial damage, and plays a key role in the mediation of cross‐talk between mitochondrial and nuclear compartments in specific cell types. J. Cell. Biochem. 98: 243–250, 2006. © 2006 Wiley‐Liss, Inc.
Recombinant human uteroglobin/CC10 inhibits the adhesion and migration of primary human endothelial cells via specific and saturable binding to fibronectin
Authors: Antico Giovanni , Lingen Mark W. , Sassano Antonella , Melby James , Welch Richard W. , Fiore Stefano , Pilon Aprile L. , Miele Lucio 
Published: February 2006

AbstractUteroglobin (UG) or Clara Cell 10 kDa protein (CC10) is a small, stable, epithelial secretory anti‐inflammatory protein. Uteroglobin has been shown to inhibit neointimal formation in vivo after balloon angioplasty through an unknown mechanism. An interaction between UG and plasma fibronectin (Fn) has been demonstrated in mice. Since Fn plays a key role in endothelial cell (EC) migration and angiogenesis, we investigated whether recombinant human UG (rhUG) affects EC migration via Fn binding. In this report, we show a saturable binding of rhUG to Fn depending on Fn conformation and that rhUG is covalently cross‐linked to Fn by transglutaminase (TGase). Additionally, our study highlights that rhUG can also bind to exogenously added or self‐secreted Fn on the membrane of human primary microvascular endothelial cells (HMVEC), although these complexes are weakly associated with the plasmalemma. Upon the interaction with Fn in solid phase, rhUG strongly inhibits HMVEC attachment on Fn, but not on other ECM proteins. Consequently, rhUG also inhibits cell migration in a dose dependent fashion (I.C.50 = 65 nM) and hinders the “wound healing” in vitro. The small size, stability and human tolerability of rhUG suggest that rhUG in slow‐release form or genetically delivered could be used in humans to modulate cell/Fn interactions in the context of tumor microenvironment or in the context of inflammation and fibrosis. J. Cell. Physiol. 207: 553–561, 2006. © 2006 Wiley‐Liss, Inc.
Interleukin‐1 beta induction of matrix metalloproteinase‐1 transcription in chondrocytes requires ERK‐dependent activation of CCAAT enhancer‐binding protein‐beta
Authors: Raymond Lauren , Eck Sarah , Mollmark Jessica , Hays Ezra , Tomek Ivan , Kantor Stephen , Elliott Sarah , Vincenti Matthew 
Published: February 2006

AbstractInterleukin‐1 beta (IL‐1β) is a central mediator of inflammation and connective tissue destruction in rheumatoid arthritis. IL‐1β activates articular chondrocytes to produce matrix metalloproteinase‐1 (MMP‐1), an enzyme capable of dismantling the collagen scaffold of articular cartilage. To define the transcription factors and signaling intermediates that activate MMP‐1 transcription in chondrocytes, we performed transient transfection of MMP‐1 promoter constructs followed by reporter assays. These studies identified an IL‐1β‐responsive region of the human MMP‐1 promoter that contains a consensus CCAAT enhancer‐binding protein (C/EBP) binding site. Deletion of this site reduced overall transcriptional activity of the MMP‐1 promoter, as well as decreased fold induction by IL‐1β. IL‐1β stimulation of chondrocytes increased binding of C/EBP‐β to the MMP‐1 C/EBP site. Extracellular signal regulated kinase (ERK) pathway‐dependent phosphorylation of C/EBP‐β on threonine 235 activates this transcription factor. Here we show that IL‐1β stimulation of chondrocytes induced phosphorylation of C/EBP‐β on threonine 235, and that the ERK pathway inhibitor PD98059 reduced this phosphorylation. We further show that PD98059 reduces IL‐1β‐induced MMP‐1 mRNA expression in chondrocytes. Moreover, inhibition of the ERK pathway by expression of dominant‐negative forms of ERK1 and ERK2 impaired the ability of IL‐1β to transactivate the MMP‐1 promoter. Our findings demonstrate a novel role for C/EBP‐β in IL‐1β‐induced connective tissue disease and define a new nuclear target for the ERK pathway in MMP‐1 gene activation. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Src oncogene activates MMP‐2 expression via the ERK/Sp1 pathway
Authors: Kuo LunYu , Chang Hui‐Chiu , Leu Tzeng‐Horng , Maa Ming‐Chie , Hung Wen‐Chun 
Published: February 2006

AbstractPrevious studies demonstrated that activation of Src oncogene increased matrix metalloproteinase‐2 (MMP‐2) expression in various types of cells. In this study, we elucidated the underlying mechanism of Src‐induced MMP‐2. We first used murine fibroblast cell line C3H10T1/2 and its v‐Src transfectant IV5 to address this issue. RT‐PCR and promoter activity assay indicated that Src stimulated MMP‐2 via transcriptional activation. Transfection of constitutively active Src into C3H10T1/2 cells also stimulated MMP‐2 mRNA expression. Deletion and mutation analysis indicated that the Sp1 site located within the −91/−84 region of human MMP‐2 promoter is the major responsive element for Src. Electrophoresis mobility shift assays showed that Src enhanced the binding of Sp1 to this consensus site to stimulate MMP‐2 gene expression. We next investigated the signaling pathway that mediated the effect of Src on MMP‐2. Our data showed that extracellular signal‐regulated kinase (ERK) pathway inhibitor PD98059, but not the c‐Jun N‐terminal kinase (JNK) inhibitor SP600125, p38 kinase inhibitor SB203580, and PI3K inhibitor wortmannin, attenuated Src‐induced MMP‐2 promoter activity. These inhibitors did not show significant effect on basal MMP‐2 promoter activity in C3H10T1/2 cells. In addition, the dominant negative mutant of ERK‐2 suppressed the activation of MMP‐2 by Src. Treatment of PD98059 or an Src specific inhibitor PP1 reduced Sp1 DNA binding activity in IV5 cells. Taken together, our results strongly suggest that Src induces MMP‐2 expression via transcription activation and the ERK/Sp1 signaling pathway is involved in this process. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Off‐line combination of reversed‐phase liquid chromatography and laser desorption/ionization time‐of‐flight mass spectrometry with seamless post‐source decay fragment ion analysis for characterization of square‐planar nickel(II) complexes
Authors: Řehulka Pavel , Popkov Alexander , Nádvorník Milan , Planeta Josef , Mazanec Karel , Chmelík Josef 
Published: February 2006

AbstractCharacterization of square‐planar nickel(II) complexes of the Schiff base of (S)‐N‐benzylproline (2‐benzoylphenyl)amide and various amino acids that are used as efficient α‐amino acids synthons was carried out using laser desorption/ionization time‐of‐flight mass spectrometry (LDI‐TOF MS) in off‐line combination with liquid chromatography. A mixture of four square‐planar nickel(II) complexes was separated using reversed‐phase liquid chromatography (RPLC) and the separated fractions from the chromatographic run were spotted on the metal target directly from the column outlet using a lab‐made sample deposition device. The separated fractions were then analyzed by LDI‐TOF MS. Seamless postsource decay (sPSD) fragment ion analysis was used for their structural characterization, which made possible the confirmation of expected chemical structures of the analyzed compounds. The off‐line combination of the separation by RPLC and analysis by LDI‐TOF MS allowed successful separation, sensitive detection and structure elucidation of the square‐planar nickel(II) complexes. Copyright © 2006 John Wiley & Sons, Ltd.
Analysis of fungal cyclopentenone derivatives from Hygrophorus spp. by liquid chromatography/electrospray‐tandem mass spectrometry
Authors: Lübken Tilo , Arnold Norbert , Wessjohann Ludger , Böttcher Christoph , Schmidt Jürgen 
Published: February 2006

AbstractFruitbodies of the genus Hygrophorus (Basidiomycetes) contain a series of anti‐biologically active compounds. These substances named hygrophorones possess a cyclopentenone skeleton. LC/ESI‐MS/MS presents a valuable tool for the identification of such compounds. The mass spectral behaviour of typical selected members of this group under positive and negative ion electrospray conditions is discussed. Using the ESI collision‐induced dissociation (CID) mass spectra of the [M + H]+ and [M − H]− ions, respectively, the compounds can be classified with respect to the substitution pattern at the cyclopentenone ring and the type of oxygenation at C‐6 (hydroxy/acetoxy or oxo function) of the side chain. The elemental composition of the fragment ions was determined by ESI‐QqTOF measurements. Thus, in case of the negative ion CID mass spectra an unusual loss of CO2 from the deprotonated molecular ions could be observed. Copyright © 2006 John Wiley & Sons, Ltd.
Canine ACL fibroblast integrin expression and cell alignment in response to cyclic tensile strain in three‐dimensional collagen gels
Authors: Henshaw D. Ross , Attia Erik , Bhargava Madhu , Hannafin Jo A. 
Published: February 2006

AbstractTissue‐engineered ligament substitutes have the potential to become an alternative graft source for ligament reconstruction. If this approach is to become viable, one must first understand and define the mechanisms responsible for creation, maintenance, and remodeling of the native anterior cruciate ligament. It is well accepted that mechanical load alters fibroblast phenotypic expression in a variety of cell sources; however, the mechanosensitive pathways responsible for alteration in matrix production, remodeling, and alignment are unknown. We hypothesize that cell surface integrins play a role in this mechanotransduction process, and as such respond to application of cyclic tensile load. Linear 3D collagen gels containing canine ACL fibroblasts were created in Flexercell Tissue‐Train Culture Plates. Gels were untethered (control), tethered without external strain (tethered), or tethered and exposed to 2.5% cyclic strain for 2 h per day for 4 days (strain). Quantitation of α1, α5, and β1 integrin subunit was performed using flow cytometry. Cell and matrix alignment was studied using light, polarized light, and fluorescent microscopy. Expression of α5 and β1 integrin subunits was increased significantly in fibroblasts in tethered and strained 3D collagen gels compared with the control, unloaded constructs (p < 0.05). These integrins are known to function as mechanotransducers in other tissues, implicating a similar role in mechanotransduction in ACL fibroblasts. Histologic analysis of the tethered and strained gels demonstrated a linear arrangement of cells and parallel collagen fibril architecture. In contrast, cell distribution and collagen alignment were disorganized in the control, unloaded gels. The alignment of cells and collagen in the 3D gels parallel to applied strain is similar to the in vivo state. These data add to our understanding of the behavior of ACL fibroblasts in vitro. The ability to manipulate signal transduction pathways may enhance our ability to engineer implantable ACL grafts or to modify ACL healing response. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:481–490, 2006
The effect of thrombin on ACL fibroblast interactions with collagen hydrogels
Authors: Murray M.M. , Forsythe B. , Chen F. , Lee S.J. , Yoo J.J. , Atala A. , Steinert A. 
Published: February 2006

AbstractPremature loss of provisional scaffold formation has been identified as one of the factors responsible for poor healing of intraarticular tissues. To address this deficiency, substitute provisional scaffolds are being developed. The function of these scaffolds can be enhanced by the addition of specific extracellular matrix proteins. In this study, it was hypothesized that the addition of thrombin to a provisional scaffold material would result in increases in cell proliferation, collagen production, and cell migration within the scaffold. These three parameters are thought to be critical components of wound healing. Gels containing fibrin and collagen supplemented with either 0, 10.5, 21, or 42 U/mL of thrombin were placed in contact with explants of tissue from the anterior cruciate ligament. The addition of thrombin stimulated cell migration at low concentrations and impaired migration at higher concentrations, and had no significant effect on cell proliferation or collagen production. The use of all concentrations of thrombin resulted in mechanically weaker gels. Thus, the use of thrombin to optimize a collagen‐platelet rich plasma (PRP) provisional scaffold must be done with caution, and use of high concentrations of thrombin (>42 IU/mL) should be avoided specifically in situations where gel strength or cell ingrowth is important. Use of low concentrations of thrombin (10.5 IU/mL) may be beneficial in applications where a faster set time and enhanced cell migration are desirable and the gel mechanical strength is of secondary importance. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:508–515, 2006
When service fails: The role of the salesperson and the customer
Authors: Chang Chia‐Chi 
Published: February 2006

AbstractService failures and consequent recoveries have been identified as a critical determinant of customer retention. Hence, effective service recovery programs warrant further exploration. In particular, with the current emphasis on relationship selling, salespeople should learn how to improvise to serve their customers effectively, including solving problems when service failure occurs. Therefore, alternatives to current common practices in industry should be investigated. The results of the present study suggest that by providing customers a choice of service recovery options, salespeople can augment customers' sense of control and ultimately their satisfaction with the service recovery and the overall service transaction. The investigation also proposed that customer satisfaction would be contingent upon the importance of the service. However, study findings revealed that this was not the case. Implications of the findings are also discussed. © 2006 Wiley Periodicals, Inc.
Overcoming the illusion of will and self‐fabrication: Going beyond naïve subjective personal introspection to an unconscious/conscious theory of behavior explanation
Authors: Woodside Arch G. 
Published: February 2006

AbstractNaïve subjective personal introspection includes the failure to recognize the confirmability of one's own attitudes and personal meanings learned explicitly from self‐examining such topics and explaining one's own behavior. Unconscious/conscious theory of behavior explanation follows from unifying the research on unintended thought–behavior with folk explanations of behavior. This article describes advances in research confirming own attitudes and personal meaning and suggests the need for applying multiple methods to overcome the fundamental attribution error, inherent cultural prejudices, and the general bias toward self‐fabrication. The discussion is valuable for achieving a deep understanding of how customers think, advancing from subjective to confirmatory personal introspection, and understanding the need to apply research tools useful for enlightening knowledge and overcoming the inherent bias within subjective personal introspection. © 2006 Wiley Periodicals, Inc.
Blood donations, iron stores, and risk of Parkinson's disease
Authors: Logroscino Giancarlo , Chen Honglei , Wing Al , Ascherio Alberto 
Published: February 2006

AbstractIron overload and systemic iron stores may be important in the pathogenesis of Parkinson's disease (PD). We therefore examined the association between blood donations, which reduce body iron stores, and risk of PD in the Health Professionals Follow‐Up Study, a large cohort investigation of U.S. men. Our hypothesis was that blood donation reduces the risk of PD by lowering systemic iron stores. Although the number of blood donations was inversely related to the ferritin levels in a subsample of the study population, no association was found between the number of blood donations and risk of PD (P for trend = 0.6). Unexpectedly, the risk of PD was higher among men who reported recent multiple blood donations (P for trend = 0.05). The results of this study do not support the hypothesis that reduced systemic iron stores lower the risk of PD. © 2006 Movement Disorder Society
Automatic selection of arterial input function using cluster analysis
Authors: Mouridsen Kim , Christensen Søren , Gyldensted Louise , Østergaard Leif 
Published: February 2006

AbstractQuantification of cerebral blood flow (CBF) using dynamic susceptibility contrast MRI requires determination of the arterial input function (AIF) representing the delivery of intravascular tracer to tissue. This is typically accomplished manually by inspection of concentration time curves (CTCs) in regions containing the ICA, VA, and MCA. This is, however, a time consuming and operator dependent procedure. We suggest a completely automatic procedure for establishing the AIF based on a cluster analysis algorithm. In 20 normal subjects CBF maps calculated in 2 slices by the automatic procedure were compared to maps obtained with AIFs selected individually by 7 experienced operators. The average manual to automatic CBF ratio was 1.03 ± 0.15 in the lower slice and 1.05 ± 0.12 in the upper slice, demonstrating excellent agreement between the manual and automatic method. The algorithm provides means for objectively assessing AIF candidates in local AIF search algorithms designed to reduce bias due to delay and dispersion. Given the reproducibility and speed (10 s) of the automatic method, we speculate that it will greatly improve the accuracy of perfusion images and facilitate their use in clinical diagnosis and decision‐making, particularly in acute stroke but also in cerebrovascular disease in general. Magn Reson Med, 2006. © 2006 Wiley‐Liss, Inc.