bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lipopolysaccharide induces autophagy through BIRC2 in human umbilical vein endothelial cells
Authors: Meng Ning , Wu LingLing , Gao JianGang , Zhao Jing , Su Le , Su Hua , Zhang ShangLi , Miao JunYing 
Published: May 2010

AbstractLipopolysaccharide (LPS), as an important proinflammatory agent, targets the endothelium. However, almost all in vitro experiments of the effect of LPS on vascular endothelial cells (VECs) were performed under an artificially decreased concentration of serum that was not enough to maintain the cell growth for a long time. The mechanism underlying LPS action on VECs cultured in a nutrient‐rich condition is not clear. To address this question and mimic the in vivo condition, we investigated the effect of LPS on VEC autophagy, which is involved in numerous physiological processes. The effect of LPS on microtubule‐associated protein 1 light chain 3 (LC3) distribution, LC3‐II accumulation and p62 degradation showed that LPS effectively induced autophagy in VECs cultured in the presence of 20% serum. To understand the mechanism by which LPS triggers the cell autophagy, we first investigated the effects of LPS on the expression of BIRC2 (cIAP1), a well‐known apoptosis inhibitor, and on the kinase activity of mammalian target of rapamycin (mTOR) and nuclear translocation of p53. LPS increased BIRC2 expression in a dose‐ and time‐dependent manner and elevated the intranuclear level of p53 but had no effect on the mTOR pathway when it triggered VEC autophagy. Furthermore, knockdown of BIRC2 by RNA interference inhibited the autophagy and the translocation of p53 to nuclei induced by LPS. These data suggest a novel role for BIRC2 in LPS‐induced autophagy in VECs. J. Cell. Physiol. 225: 174–179, 2010. © 2010 Wiley‐Liss, Inc.
TRUSS, TNF‐R1, and TRPC ion channels synergistically reverse endoplasmic reticulum Ca2+ storage reduction in response to m1 muscarinic acetylcholine receptor signaling
Authors: Mace Kimberly E. , Lussier Marc P. , Boulay Guylain , Terry‐Powers Jennifer L. , Parfrey Helen , Perraud Anne‐Laure , Riches David W.H. 
Published: May 2010

AbstractAlthough most signaling responses initiated by tumor necrosis factor‐α (TNF‐α) occur in a Ca2+‐independent fashion, TNF‐α receptor signaling augments Ca2+ entry induced by Gαq/11 G‐protein coupled receptors (GPCRs) in endothelial cells and increases trans‐endothelial permeability. The signaling events involved in GPCR‐induced Ca2+ influx have been characterized and involve store‐operated Ca2+ entry facilitated by the Ca2+ permeable ion channel, transient receptor potential canonical 4 (TRPC4). Little is known about the mechanisms by which TNF‐α receptor signaling augments GPCR‐induced Ca2+ entry. TNF‐α Receptor Ubiquitous Signaling and Scaffolding protein (TRUSS) is a tumor necrosis factor receptor‐1 (TNF‐R1)‐associated protein whose gene name is TRPC4‐associated protein (TRPC4AP). The goal of our study was to test the hypothesis that TRUSS serves to link TNF‐R1 and GPCR‐signaling pathways at the level of TRPC4 by: (i) determining if TRUSS and TNF‐R1 interact with TRPC4, and (ii) investigating the role of TRUSS, TNF‐R1, and TRPC4 in GPCR‐induced Ca2+ signaling. Here, we show that TRUSS and TNF‐R1 interact with a sub‐family of TRPC channels (TRPC1, 4, and 5). In addition, we show that TRUSS and TNF‐R1 function together with TRPC4 to elevate endoplasmic reticulum Ca2+ filling in the context of reduced endoplasmic reticulum Ca2+ storage initiated by G‐protein coupled m1 muscarinic acetylcholine receptor (m1AchR) signaling. Together, these findings suggest that TNF‐R1, TRUSS, and TRPC4 augment Ca2+ loading of endoplasmic reticulum Ca2+ stores in the context of m1AchR stimulation and provide new insights into the mechanisms that connect TNF‐R1 to GPCR‐induced Ca2+ signaling. J. Cell. Physiol. 225: 444–453, 2010. © 2010 Wiley‐Liss, Inc.
Centrosome biogenesis continues in the absence of microtubules during prolonged S‐phase arrest
Authors: Collins Elizabeth S. , Hornick Jessica E. , Durcan Thomas M. , Collins Nicholas S. , Archer William , Karanjeet Kul B. , Vaughan Kevin T. , Hinchcliffe Edward H. 
Published: May 2010

AbstractWhen CHO cells are arrested in S‐phase, they undergo repeated rounds of centrosome duplication without cell‐cycle progression. While the increase is slow and asynchronous, the number of centrosomes in these cells does rise with time. To investigate mechanisms controlling this duplication, we have arrested CHO cells in S‐phase for up to 72 h, and coordinately inhibited new centriole formation by treatment with the microtubule poison colcemid. We find that in such cells, the pre‐existing centrosomes remain, and a variable number of foci—containing α/γ‐tubulin and centrin 2—assemble at the nuclear periphery. When the colcemid is washed out, the nuclear‐associated foci disappear, and cells assemble new centriole‐containing centrosomes, which accumulate the centriole scaffold protein SAS‐6, nucleate microtubule asters, and form functional mitotic spindle poles. The number of centrosomes that assemble following colcemid washout increases with duration of S‐phase arrest, even though the number of nuclear‐associated foci or pre‐existing centrosomes does not increase. This suggests that during S‐phase, a cryptic generative event occurs repeatedly, even in the absence of new triplet microtubule assembly. When triplet microtubule assembly is restored, these cryptic generative events become realized, and multiple centriole‐containing centrosomes assemble. J. Cell. Physiol. 225: 454–465, 2010. © 2010 Wiley‐Liss, Inc.
Articular cartilage repair with autologous bone marrow mesenchymal cells
Authors: Matsumoto Tomiya , Okabe Takahiro , Ikawa Tesshu , Iida Takahiro , Yasuda Hiroyuki , Nakamura Hiroaki , Wakitani Shigeyuki 
Published: May 2010

AbstractArticular cartilage defects that do not repair spontaneously induce osteoarthritic changes in joints over a long period of observation. In this study, we examined the usefulness of transplanting culture‐expanded bone marrow mesenchymal cells into osteochondral defects of joints with cartilage defects. First, we performed experiments on rabbits and up on obtaining good results proceeded to perform the experiments on humans. Macroscopic and histological repair with this method was good, and good clinical results were obtained although there was no significant difference with the control group. Recent reports have indicated that this procedure is comparable to autologous chondrocyte implantation, and concluded that it was a good procedure because it required one step less than that required by surgery, reduced costs for patients, and minimized donor site morbidity. Although some reports have previously shown that progenitor cells formed a tumor when implanted into immune‐deficient mice after long term in vitro culture, the safety of the cell transplantation was confirmed by our clinical experience. Thus, this procedure is useful, effective, and safe, but the repaired tissues were not always hyaline cartilage. To obtain better repair with this procedure, treatment approaches using some growth factors during in vitro culture or gene transfection are being explored. J. Cell. Physiol. 225: 291–295, 2010. © 2010 Wiley‐Liss, Inc.
Regulation of osteoblast and osteoclast functions by FGF‐6
Authors: Bosetti Michela , Leigheb Massimiliano , Brooks Roger A. , Boccafoschi Francesca , Cannas Mario F. 
Published: May 2010

AbstractFibroblast growth factor‐6 (FGF‐6) is known to be the key ligand for fibroblast growth factor receptor 4 (FGFR4) during muscle regeneration but its role in bone has yet to be verified. FGFR signaling is known to be important in the initiation and regulation of osteogenesis, so in this study the actions of FGF‐6 on human osteoblasts and osteoclasts were investigated. Human primary osteoblasts (hOB) were used to study the effect of FGF‐6 on proliferation (by ATP quantification), signal transduction (by ERK and AKT phosphorylation), differentiation (by alkaline phosphatase activity, APA), and mineralization (by calcein staining). To study FGF‐6 activity on osteoclast differentiation, human bone marrow cells were used and tartrate‐resistant acid phosphatase (TRAP) multinucleated cells together with actin filaments arrangements were quantified. Human primary mature osteoclasts were used to evaluate the effect of FGF‐6 on osteoclast reabsorbing activity by reabsorbed pit measurements. FGF‐6 >10−9 M as FGF‐2 10−7 M induced hOB proliferation mediated by pERK together with a reduction in APA and reduced mineralization of the treated cells. Moreover FGF‐6 increased the formation of TRAP‐positive multinucleated cells in a dose‐dependent manner (maximal effect at 10−8 M). FGF‐6‐treated cells showed also a greater percentage of cells that formed typical osteoclast sealing zones. Mature osteoclasts cultured on dentine slice increased the area of reabsorption with a maximal effect of FGF‐6 at 10−12 M. FGF‐6 may be considered a regulator of bone metabolism as shown by its activity on both osteoblasts and osteoclasts. J. Cell. Physiol. 225: 466–471, 2010. © 2010 Wiley‐Liss, Inc.
Disruption of the hedgehog signaling pathway contributes to the hair follicle cycling deficiency in Vdr knockout mice
Authors: Teichert Arnaud , Elalieh Hashem , Bikle Daniel 
Published: May 2010

AbstractMice null for the Vitamin D receptor (VdrKO) have a disrupted first hair follicle cycle and aborted subsequent hair follicle cycling. We examined the expression of different markers and mediators of hair follicle cycling in the hair follicle of the VdrKO mouse during days 13–22 when the hair follicle normally initiates and completes the first catagen. We compared the expression of those genes in mice with a nonsense mutation in hairless (Rhino), which have a similar alopecia phenotype, and to Cyp27b1 null mice which are deficient in the production of 1,25(OH)2D3, the Vdr ligand, but display normal hair follicle cycling. Our results demonstrate the down regulation of hair follicle markers and the alteration of expression of hedgehog (Hh), Wnt, Fgf, and Tgfβ pathways in VdrKO and Rhino mice, but not in Cyp27b1KO mice. Treatment of VdrKO mice with an agonist to the Hh pathway partially restored hair follicle cycling, suggesting a role of this pathway in the regulation of hair follicle cycling by VDR. These results suggest that Vdr regulates directly or indirectly the expression of genes required for hair follicle cycling, including Hh signaling, independent of 1,25(OH)2D3. J. Cell. Physiol. 225: 482–489, 2010. © 2010 Wiley‐Liss, Inc.
MicroRNA‐1 inhibits myocardin‐induced contractility of human vascular smooth muscle cells
Authors: Jiang Yulan , Yin Hao , Zheng Xi‐Long 
Published: May 2010

AbstractMyocardin, a cofactor of serum response factor (SRF), specifically induces the expression of contractile proteins to promote differentiation and contractile phenotype of smooth muscle cells (SMCs). SRF directly induces the transcription of microRNA‐1 (miR‐1) in cardiac and skeletal muscle precursor cells and miR‐1 promotes the skeletal muscle differentiation and modulates cardiac hypertrophy. We aimed to examine whether miR‐1 plays a role in the regulation of smooth muscle contractility. We found that miR‐1 expression was induced by myocardin overexpression in human aortic SMCs. In a collagen lattice contraction assay using SMCs harboring a doxycycline‐inducible expression system for myocardin, we found that myocardin expression increased the contractility of SMCs, which was significantly inhibited by exogenous miR‐1. Our further studies revealed that exogenous miR‐1, which did not affect myocardin or SRF expression, suppressed the expression of contractile proteins, such as α‐SMA and SM22, and impaired the actin cytoskeletal organization. Taken together, our results have revealed that myocardin induces miR‐1 expression, which represses the expression of contractile proteins and thereby inhibits the contractility of SMCs. Therefore, our findings suggest a role of miR‐1 in the negative feedback loop in the regulation of contractility induced by myocardin. J. Cell. Physiol. 225: 506–511, 2010. © 2010 Wiley‐Liss, Inc.
RETRACTED: Impact of histone deacetylase inhibitors SAHA and MS‐275 on DNA repair pathways in human mesenchymal stem cells
Authors: Di Bernardo Giovanni , Alessio Nicola , Dell'Aversana Carmela , Casale Fiorina , Teti Diana , Cipollaro Marilena , Altucci Lucia , Galderisi Umberto 
Published: May 2010

AbstractHistone deacetylase inhibitors (HDACis) have received considerable attention for their anti‐tumoral properties. We report here the effects of two HDACis, SAHA and MS‐275, on the biology of mesenchymal stem cells (MSCs). It is well known that HDACis trigger both DNA damage responses and actual DNA damage in cancer cells. On this premise, we evaluated HDACis influence on DNA damage pathways in MSCs. We analyzed a panel of genes involved in the regulation of base and nucleotide excision repair, mismatch repair, and double strand break repair. That a majority of the analyzed genes displayed significant expression changes upon incubation with SAHA or MS‐275 suggested that regulation of their expression is greatly affected by HDACis. The complex expression pattern, with some genes up‐regulated and other under‐expressed, did not allow to foresee whether these changes allow cells cope with stressful DNA damaging stimuli. Furthermore, we evaluated the biological outcome following treatment of MSCs with DNA damaging agents (H2O2 and UV) in presence of HDACis. In these settings, MSCs treated with H2O2 or UV radiation underwent apoptosis and/or senescence, and pre‐incubation with HDACi exacerbated cell death phenomena. Accordingly, the number of cells harboring 8‐oxo‐7,8‐dihydroguanine (8oxodG), a hallmark of DNA oxidative damage, was significantly higher in samples incubated with HDACis compared to controls. In summary, our findings suggest that SAHA and MS‐275, even at low effective doses, can alter the biology of MSCs, diminishing their ability to survive the effects of DNA‐damaging agents. J. Cell. Physiol. 225: 537–544, 2010. © 2010 Wiley‐Liss, Inc.
In vitro differentiation of unrestricted somatic stem cells into functional hepatic‐like cells displaying a hepatocyte‐like glucose metabolism
Authors: Waclawczyk Simon , Buchheiser Anja , Flögel Ulrich , Radke Teja F. , Kögler Gesine 
Published: May 2010

AbstractThe hepatic‐like phenotype resulting from in vitro differentiation of unrestricted somatic stem cells (USSC) derived from human umbilical cord blood (CB) was analyzed with regard to functional and metabolic aspects. USSC can be differentiated into cells of all three germ layers in vitro and in vivo and, although they share many features with mesenchymal stroma cells (MSC), can be distinguished from these by their expression of DLK1 as well as a restricted adipogenic differentiation potential. For the differentiation procedure described herein, a novel three‐stage differentiation protocol resembling embryonic developmental processes of hepatic endoderm was applied. Hepatic pre‐induction was performed by activinA and FGF4 resulting in enhanced SOX17 and FOXA2 expression. Further differentiation was achieved sequentially by retinoic acid, FGF4, HGF, EGF, and OSM resulting in a hepatic endodermal identity, characterized by the expression of AFP and HNF1α. Thereafter, expression of G6PC, ARG1, FBP1, and HNF4α was observed, thus indicating progressive differentiation. Functional studies concerning albumin secretion, urea formation, and cytochrome‐p450‐3A4 (CYP3A4) enzyme activity confirmed the hepatic‐like phenotype. In order to characterize the differentiated cells at a metabolic level, USSC were incubated with [1‐13C]glucose. By tracing the fate of the molecule's label via isotopomer analysis using 13C NMR spectroscopy, formation of both glycogen and some gluconeogenetic activity could be observed providing evidence of a hepatocyte‐like glucose metabolism in differentiated USSC. In conclusion, the results of the present study indicate that USSC represent a stem cell source with a substantial hepatic differentiation capacity which hold the potential for clinical applications. J. Cell. Physiol. 225: 545–554, 2010. © 2010 Wiley‐Liss, Inc.
Food safety and consumer willingness to pay for certified traceable food in China
Authors: Xu Lingling , Wu Linhai 
Published: May 2010

AbstractBACKGROUND: The September 2008 melamine outbreak in China has adversely affected perceptions of food safety among consumers. This paper presents a survey of the perception of food safety and willingness to pay for certified traceable (CT) food among the citizens of Jiangsu Province. It presents the critical necessity of establishing a food traceability system (FTS) to address possible similar outbreaks in the future.RESULTS: The results show that 36% of the respondents are strongly dissatisfied with food safety conditions in the province. Only 37% of the respondents have heard of FTS. Among the respondents who chose to buy CT food, 32% were unwilling to shoulder the extra cost. The consumers' overall satisfaction with food safety, awareness of FTS, gender, age, educational level and income are the main determinants of Chinese consumers' willingness to pay for CT food.CONCLUSION: Based on the results, it is proposed that the Chinese government pay attention to the mentality of its citizens when establishing an FTS and take measures to lift consumers' willingness to pay for CT food. Results of this study will provide valuable insights to developing countries. Copyright © 2010 Society of Chemical Industry
Iterative Shannon Entropy – a Methodology to Quantify the Information Content of Value Range Dependent Data Distributions. Application to Descriptor and Compound Selectivity Profiling
Authors: Wassermann Anne Mai , Vogt Martin , Bajorath Jürgen 
Published: May 2010

AbstractWe introduce an entropy‐based methodology, Iterative Shannon entropy (ISE), to quantify the information contained in molecular descriptors and compound selectivity data sets taking data spread directly into account. The method is applicable to determine the information content of any value range dependent data distribution. An analysis of descriptor information content has been carried out to explore alternative binning schemes for entropy calculation. Using this entropic measure we have profiled 153 compound selectivity data sets for combinations of 68 target proteins belonging to 10 target families. With the ISE measure, we aim to assign high information content to compound data sets that span a wide range of selectivity values and different selectivity relationships and hence correspond to more than one biological phenotype. Target families with high average entropy scores are identified. For members of these families, active compounds display highly differentiated selectivity profiles.
Tensor kernels for simultaneous fiber model estimation and tractography
Authors: Rathi Yogesh , Malcolm James G. , Michailovich Oleg , Westin Carl‐Fredrik , Shenton Martha E. , Bouix Sylvain 
Published: May 2010

AbstractThis paper proposes a novel framework for joint orientation distribution function estimation and tractography based on a new class of tensor kernels. Existing techniques estimate the local fiber orientation at each voxel independently so there is no running knowledge of confidence in the measured signal or estimated fiber orientation. In this work, fiber tracking is formulated as recursive estimation: at each step of tracing the fiber, the current estimate of the orientation distribution function is guided by the previous. To do this, second‐and higher‐order tensor‐based kernels are employed. A weighted mixture of these tensor kernels is used for representing crossing and branching fiber structures. While tracing a fiber, the parameters of the mixture model are estimated based on the orientation distribution function at that location and a smoothness term that penalizes deviation from the previous estimate along the fiber direction. This ensures smooth estimation along the direction of propagation of the fiber.In synthetic experiments, using a mixture of two and three components it is shown that this approach improves the angular resolution at crossings. In vivo experiments using two and three components examine the corpus callosum and corticospinal tract and confirm the ability to trace through regions known to contain such crossing and branching. Magn Reson Med, 2010. © 2010 Wiley‐Liss, Inc.
Interleukin‐9 polymorphism in infants with respiratory syncytial virus infection: An opposite effect in boys and girls
Authors: Schuurhof Annemieke , Bont Louis , Siezen Christine L. E. , Hodemaekers Hennie , van Houwelingen Hans C. , Kimman Tjeerd G. , Hoebee Barbara , Kimpen Jan L. L. , Janssen Riny 
Published: May 2010

AbstractThe predominance of severe respiratory syncytial virus (RSV) bronchiolitis in boys compared to girls is well known, but its mechanism is not yet understood. This is the first study focusing on gender‐specific genetic factors affecting the risk of severe RSV infection using a previously described cohort. We determined 347 single‐nucleotide polymorphisms (SNPs) in 470 children hospitalized for RSV infection, their parents, and 1,008 random population controls. We tested if these SNPs exerted a different effect in boys and girls by performing statistical interaction tests. Only one SNP (rs2069885) had a gender‐specific significant association with RSV infection, severe enough to require hospitalization (P‐value 0.00057). The major allele of this structural polymorphism in the interleukin (IL)‐9 gene is associated with an increased susceptibility to severe RSV infection in boys, while there is a decreased susceptibility in girls. Haplotype analysis of two SNPs in the IL‐9 gene (rs2069885 and rs1799962) showed overrepresentation of the TT haplotype in girls with severe RSV bronchiolitis requiring hospitalization indicating that this is the haplotype conferring the highest risk in girls. In conclusion, the IL‐9 genetic polymorphism (rs2069885) has an opposite effect on the risk of severe RSV bronchiolitis in boys and girls. Although so far a difference in IL‐9 production in boys and girls has not been reported, this study may help in explaining the different risks of severe RSV bronchiolitis in boys and girls. Pediatr Pulmonol. 2010; 45:608–613. © 2010 Wiley‐Liss, Inc.
Dipolar glass phase in ferrielectrics: CuInP2S6 and Ag0.1Cu0.9InP2S6 crystals
Authors: Dziaugys Andrius , Banys Juras , Macutkevic Jan , Sobiestianskas Ricardas , Vysochanskii Yulian 
Published: May 2010

AbstractThe dielectric properties of CuInP2S6 and Ag0.1Cu0.9InP2S6 crystals were investigated in wide frequency (20 Hz–3 GHz) and temperature ranges (25–360 K). The low frequencies dielectric spectra at high temperatures are highly influenced by the high ionic conductivity. The temperature dependences of the static dielectric permittivity and the mean relaxation time reveal the first order order–disorder ferrielectric phase transition at Tc = 288 K in Ag0.1Cu0.9InP2S6. The conductivity and its activation energy exhibit only a weak change close to the ferrielectric phase transition temperature in both investigated crystals. The freezing phenomena in CuInP2S6 and Ag0.1Cu0.9InP2S6 revealed the complex dielectric permittivity behaviour characteristic for transition into dipolar glass state.