bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sphingosine kinase activity is required for myogenic differentiation of C2C12 myoblasts
Authors: Meacci Elisabetta , Nuti Francesca , Donati Chiara , Cencetti Francesca , Farnararo Marta , Bruni Paola 
Published: July 2007

AbstractSphingosine kinase (SphK) is a conserved lipid kinase that catalyzes the formation of sphingosine 1‐phosphate (S1P), an important lipid mediator, which regulates fundamental biological processes. Here, we provide evidence that SphK is required for the achievement of cell growth arrest as well as myogenic differentiation of C2C12 myoblasts. Indeed, SphK activity, SphK1 protein content and S1P formation were found to be enhanced in myoblasts that became confluent as well as in differentiating cells. Enforced expression of SphK1 reduced the myoblast proliferation rate, enhanced the expression of myogenic differentiation markers and anticipated the onset of differentiated muscle phenotype. Conversely, down‐regulation of SphK1 by specific silencing by RNA interference or overexpression of the catalytically inactive SphK1, significantly increased cell growth and delayed the beginning of myogenesis; noticeably, exogenous addition of S1P rescued the biological processes. Importantly, stimulation of myogenesis in SphK1‐overexpressing myoblasts was abrogated by treatment with short interfering RNA specific for S1P2 receptor. This is the first report of the role of endogenous SphK1 in myoblast growth arrest and stimulation of myogenesis through the formation of S1P that acts as morphogenic factor via the engagement of S1P2. J. Cell. Physiol. 214:210–220, 2008. © 2007 Wiley‐Liss, Inc.
Gap junctional intercellular communication is required to maintain embryonic stem cells in a non‐differentiated and proliferative state
Authors: Todorova Mariana G. , Soria Bernat , Quesada Ivan 
Published: July 2007

AbstractPluripotent embryonic stem (ES) cells are capable of maintaining a self‐renewal state and have the potential to differentiate into derivatives of all three embryonic germ layers. Despite their importance in cell therapy and developmental biology, the mechanisms whereby ES cells remain in a proliferative and pluripotent state are still not fully understood. Here we establish a critical role of gap junctional intercellular communication (GJIC) and connexin43 (Cx43) in both processes. Pharmacological blockers of GJIC and Cx43 down‐regulation by small interfering RNA (siRNA) caused a profound inhibitory effect on GJIC, as evidenced by experiments of fluorescence recovery after photobleaching. This deficient intercellular communication in ES cells induced a loss of their pluripotent state, which was manifested in morphological changes, a decrease in alkaline phosphatase activity, Oct‐3/4 and Nanog expression, as well as an up‐regulation of several differentiation markers. A decrease in the proliferation rate was also detected. Under these conditions, the formation of embryoid bodies from mouse ES cells was impaired, although this inhibition was reversible upon restoration of GJIC. Our findings define a major function of GJIC in the regulation of self‐renewal and maintenance of pluripotency in ES cells. J. Cell. Physiol. 214: 354–362, 2008. © 2007 Wiley‐Liss, Inc.
Prostaglandin E2 upregulates EGF‐stimulated signaling in mitogenic pathways involving Akt and ERK in hepatocytes
Authors: Dajani Olav F. , Meisdalen Kristin , Guren Tormod K. , Aasrum Monica , Tveteraas Ingun Heiene , Lilleby Peggy , Thoresen G. Hege , Sandnes Dagny , Christoffersen Thoralf 
Published: July 2007

AbstractProstaglandins (PGs) such as PGE2 enhance proliferation in many cells, apparently through several distinct mechanisms, including transactivation of the epidermal growth factor (EGF) receptor (EGFR) as well as EGFR‐independent pathways. In this study we found that in primary cultures of rat hepatocytes PGE2 did not induce phosphorylation of the EGFR, and the EGFR tyrosine kinase blockers gefitinib and AG1478 did not affect PGE2‐stimulated phosphorylation of ERK1/2. In contrast, PGE2 elicited EGFR phosphorylation and EGFR tyrosine kinase inhibitor‐sensitive ERK phosphorylation in MH1C1 hepatoma cells. These findings suggest that PGE2 elicits EGFR transactivation in MH1C1 cells but not in hepatocytes. Treatment of the hepatocytes with PGE2 at 3 h after plating amplified the stimulatory effect on DNA synthesis of EGF administered at 24 h and advanced and augmented the cyclin D1 expression in response to EGF in hepatocytes. The pretreatment of the hepatocytes with PGE2 resulted in an increase in the magnitude of EGF‐stimulated Akt phosphorylation and ERK1/2 phosphorylation and kinase activity, including an extended duration of the responses, particularly of ERK, to EGF in PGE2‐treated cells. Pertussis toxin abolished the ability of PGE2 to enhance the Akt and ERK responses to EGF. The results suggest that in hepatocytes, unlike MH1C1 hepatoma cells, PGE2 does not transactivate the EGFR, but instead acts in synergism with EGF by modulating mitogenic mechanisms downstream of the EGFR. These effects seem to be at least in part Gi protein‐mediated and include upregulation of signaling in the PI3K/Akt and the Ras/ERK pathways. J. Cell. Physiol. 214: 371–380, 2008. © 2007 Wiley‐Liss, Inc.
Exposure of normal human melanocytes to a tumor promoting phorbol ester reverses growth suppression by transforming growth factor beta
Authors: Stavroulaki Melanthia , Kardassis Dimitris , Chatzaki Ekaterini , Sakellaris George , Lindschau Carsten , Haller Hermann , Tosca Androniki , Krasagakis Konstantin 
Published: July 2007

AbstractTransforming growth factor‐beta (TGF‐β), a potent inhibitor of normal melanocyte growth, does not significantly suppress growth of melanoma cells. The mechanism of melanocyte desensitization to TGF‐β in the transformation process remains largerly unknown. We investigated whether the tumor promoting phorbol ester 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) may induce melanocyte resistance to TGF‐β. Cell proliferation and DNA synthesis of normal human melanocytes were strongly inhibited by TGF‐β, whereas in the presence of TPA remained largerly unaffected. The inactive phorbol ester 4α‐phorbol 12,13 didecanoate did not modify the TGF‐β antiproliferative effect, whereas the diacylglycerol analog 1‐oleoyl‐2‐acetyl‐sn‐glycerol counteracted TGF‐β effects. Protein kinase C (PKC) is the major cellular receptor of tumor promoting phorbol esters. PKC‐α expression and phosphorylation were almost completely downregulated under combined treatment with TGF‐β + TPA at 24 and 72 h, as shown by immunoblots. Confocal microscopy demonstrated that TGF‐β‐induced nuclear accumulation of PKC‐α was abolished in the presence of TPA at the same time points. The selective PKC inhibitor Ro‐31‐8220 weakened the TGF‐β antiproliferative effect. Smads are central mediators for TGF‐β signal transduction. Smad‐dependent transcriptional activity was suppressed in TGF‐β‐treated melanocytes in the presence of TPA, as well as in ALK5 (constitutively active type I TGF‐β receptor)‐ or Smad3 + Smad4‐transfected melanocytes in the presence of Ro‐31‐8220. In addition, an antisense oligodeoxynucleotide against PKC‐α abolished TGF‐β‐driven Smad‐mediated transcription. These findings show that tumor promoting phorbol esters induce melanocyte resistance to TGF‐β, associated with downregulation of PKC‐α and suppression of Smad‐dependent transcription. This may represent an important mechanism for expansion of melanocytes exposed to PKC‐targeting tumor promoters. J. Cell. Physiol. 214: 363–370, 2008. © 2007 Wiley‐Liss, Inc.
Seeing the light: New insights into the molecular pathogenesis of retinal diseases
Authors: Campochiaro Peter A. 
Published: July 2007

AbstractIn the past, most treatments for retinal diseases have been empirical. Steroids and/or laser photocoagulation and/or surgery have been tried for almost every condition with little or no understanding of the underlying disease. Over the past several years vision researchers have uncovered molecular components of processes, such as visual transduction and the visual cycle, that are critical for visual function, and identified other molecules that lead to dysfunction and disease processes such as neovascularization and macular edema. It is becoming clear that dysregulation of certain molecules can have major effects on retinal structure and function. Studies in animal models have suggested that inhibiting or augmenting levels of a single molecule can have major effects in complex disease processes. Although several molecules probably contribute to neovascularization and excessive vascular permeability in the eye, blockade of vascular endothelial growth factor (VEGF) has remarkable beneficial effects in animal models that have now been proven to apply to human diseases in clinical trials. Intraocular injection of VEGF antagonists has revolutionized the treatment of choroidal neovascularization (CNV) and macular edema and serves as a model of targeted ocular pharmacotherapy. Significant progress elucidating the molecular pathogenesis of several disease processes in the eye may soon lead to new treatments following the lead of VEGF antagonists. Initial treatments that provide benefit from frequent intraocular injections are likely to be followed by sustained delivery of drugs and/or prolonged protein delivery by gene transfer. The eye has entered the era of molecular therapy. J. Cell. Physiol. 213: 348–354, 2007. © 2007 Wiley‐Liss, Inc.
Lipolysis is stimulated by PEGylated conjugated linoleic acid through the cyclic adenosine monophosphate‐independent signaling pathway in 3T3‐L1 cells: Activation of MEK/ERK MAPK signaling pathway and hyper‐secretion of adipo‐cytokines
Authors: Moon Hyun‐Seuk , Lee Hong‐Gu , Seo Ji‐Hye , Guo Ding‐Ding , Kim In‐Yong , Chung Chung‐Soo , Kim Tae‐Gyu , Choi Yun‐Jaie , Cho Chong‐Su 
Published: July 2007

AbstractWe previously reported that PEGylated conjugated linoleic acid (PCLA) as a pro‐drug treatment of cultures of 3T3‐L1 cells containing differentiated adipocytes caused de‐differentiation by downregulation of PPARγ2‐induced adipogenesis, and cell apoptosis induced by PCLA was lower than that induced by conjugated linoleic acid (CLA) owing to the biocompatible and hydrophilic properties of poly(ethylene glycol) (PEG). To further investigate our previous observations, the present study is designed to evaluate the lipolytic action of PCLA and its role in biochemical signaling pathways of 3T3‐L1 cells when compared to the CLA itself. Although both CLA and PCLA stimulated lipolysis, our results indicated a sensitivity difference between CLA and PCLA treatment: a time‐dependent effect on lipolysis and p‐extracellular signal‐related kinases (ERK) expression was observed for PCLA‐treated, but not for CLA‐treated cultures. Also, the induction by PCLA of mitogen‐activated protein kinase kinase (MEK)/ERK mitogen‐activated protein kinase (MAPK) activation was linked to secretion of adipo‐cytokines, interleukin‐6 (IL‐6), and interleukin‐8 (IL‐8), in time‐dependent manners. Interestingly, adenylyl cyclase inhibitor, 2′, 5′‐dideoxyadenosine (DDA), pre‐treatment did not prevent PCLA‐stimulated lipolysis. In fact, isoproterenol, but not PCLA, caused a significant increase in cyclic adenosine monophosphate (cAMP) levels, suggesting that the PCLA‐induced lipolysis was not mediated in the conventional cAMP‐dependent pathway and the cAMP was the intracellular mediator for isoproterenol‐induced lipolysis. Overall, our findings provide support for a role for PCLA as a pro‐drug in the regulation of metabolism in adipose tissue. J. Cell. Physiol. 214: 283–294, 2008. © 2007 Wiley‐Liss, Inc.
CFTR gene transfer to human cystic fibrosis pancreatic duct cells using a Sendai virus vector
Authors: Rakonczay Zoltán , Hegyi Péter , Hasegawa Mamoru , Inoue Makoto , You Jun , Iida Akihiro , Ignáth Imre , Alton Eric W.F.W. , Griesenbach Uta , Óvári Gabriella , Vág János , Da Paula Ana C. , Crawford Russell M. , Varga Gábor , Amaral Margarida D. , Mehta Anil , Lonovics János , Argent Barry E. , Gray Michael A. 
Published: July 2007

AbstractCystic fibrosis (CF) is a fatal inherited disease caused by the absence or dysfunction of the CF transmembrane conductance regulator (CFTR) Cl− channel. About 70% of CF patients are exocrine pancreatic insufficient due to failure of the pancreatic ducts to secrete a HCO‐rich fluid. Our aim in this study was to investigate the potential of a recombinant Sendai virus (SeV) vector to introduce normal CFTR into human CF pancreatic duct (CFPAC‐1) cells, and to assess the effect of CFTR gene transfer on the key transporters involved in HCO transport. Using polarized cultures of homozygous F508del CFPAC‐1 cells as a model for the human CF pancreatic ductal epithelium we showed that SeV was an efficient gene transfer agent when applied to the apical membrane. The presence of functional CFTR was confirmed using iodide efflux assay. CFTR expression had no effect on cell growth, monolayer integrity, and mRNA levels for key transporters in the duct cell (pNBC, AE2, NHE2, NHE3, DRA, and PAT‐1), but did upregulate the activity of apical Cl−/HCO and Na+/H+ exchangers (NHEs). In CFTR‐corrected cells, apical Cl−/HCO exchange activity was further enhanced by cAMP, a key feature exhibited by normal pancreatic duct cells. The cAMP stimulated Cl−/HCO exchange was inhibited by dihydro‐4,4′‐diisothiocyanostilbene‐2,2′‐disulfonic acid (H2‐DIDS), but not by a specific CFTR inhibitor, CFTRinh‐172. Our data show that SeV vector is a potential CFTR gene transfer agent for human pancreatic duct cells and that expression of CFTR in CF cells is associated with a restoration of Cl− and HCO transport at the apical membrane. J. Cell. Physiol. 214: 442–455, 2008. © 2007 Wiley‐Liss, Inc.
Induction of regulatory T cells by physiological level estrogen
Authors: Tai Ping , Wang Junpeng , Jin Huali , Song Xiaoming , Yan Jun , Kang Youmin , Zhao Lin , An Xiaojin , Du Xiaogang , Chen Xiufen , Wang Songbo , Xia Guoliang , Wang Bin 
Published: July 2007

AbstractNaturally occurring CD4+CD25+regulatory T cells (Treg) exert an important role in mediating maternal tolerance to the fetus during pregnancy, and this effect might be regulated via maternal estrogen secretion. Although estrogen concentration in the pharmaceutical range has been shown to drive expansion of CD4+CD25+Treg cells, little is known about how and through what mechanisms E2 within the physiological concentration range of pregnancy affects this expansion. Using in vivo and in vitro mouse models in these experiments, we observed that E2 at physiological doses not only expanded Treg cell in different tissues but also increased expression of the Foxp3 gene, a hallmark for CD4+CD25+Treg cell function, and the IL‐10 gene as well. Importantly, our results demonstrate that E2, at physiological doses, stimulated the conversion of CD4+CD25−T cells into CD4+CD25+T cells which exhibited enhanced Foxp3 and IL‐10 expression in vitro. Such converted CD4+CD25+T cells had similar regulatory function as naturally occurring Treg cells, as demonstrated by their ability to suppress naïve T cell proliferation in a mixed lymphocyte reaction. We also found that the estrogen receptor (ER) exist in the CD4+CD25−T cells and the conversion of CD4+CD25−T cells into CD4+CD25+T cells stimulated by E2 could be inhibited by ICI182,780, a specific inhibitor of ER(s). This supports that E2 may directly act on CD4+CD25−T cells via ER(s). We conclude that E2 is a potential physiological regulatory factor for the peripheral development of CD4+CD25+Treg cells during the implantation period in mice. J. Cell. Physiol. 214: 456–464, 2008. © 2007 Wiley‐Liss, Inc.
Cross‐intersecting couples of graphs
Authors: Fachini Emanuela , Körner János 
Published: July 2007

AbstractTwo graphs on the same vertex set form a cross‐intersecting couple if they have a pair of clique coverings with the property that every pair of cliques from the respective coverings intersect. In particular, a graph is called normal if it forms a cross‐intersecting couple with its complement. We determine the largest size of families of graphs every pair of which forms a cross‐intersecting couple under various additional restrictions. © 2007 Wiley Periodicals, Inc. J Graph Theory 56: 105–112, 2007
Evolution of the cephalopod head complex by assembly of multiple molluscan body parts: Evidence from Nautilus embryonic development
Authors: Shigeno Shuichi , Sasaki Takenori , Moritaki Takeya , Kasugai Takashi , Vecchione Michael , Agata Kiyokazu 
Published: July 2007

AbstractCephalopod head parts are among the most complex occurring in all invertebrates. Hypotheses for the evolutionary process require a drastic body‐plan transition in relation to the life‐style changes from benthos to active nekton. Determining these transitions, however, has been elusive because of scarcity of fossil records of soft tissues and lack of some of the early developmental stages of the basal species. Here we report the first embryological evidence in the nautiloid cephalopod Nautilus pompilius for the morphological development of the head complex by a unique assembly of multiple archetypical molluscan body parts. Using a specialized aquarium system, we successfully obtained a series of developmental stages that enabled us to test previous controversial scenarios. Our results demonstrate that the embryonic organs exhibit body plans that are primarily bilateral and antero‐posteriorly elongated at stereotyped positions. The distinct cephalic compartment, foot, brain cords, mantle, and shell resemble the body plans of monoplacophorans and basal gastropods. The numerous digital tentacles of Nautilus develop from simple serial and spatially‐patterned bud‐like anlagen along the anterior–posterior axis, indicating that origins of digital tentacles or arms of all other cephalopods develop not from the head but from the foot. In middle and late embryos, the primary body plans largely change to those of juveniles or adults, and finally form a “head” complex assembled by anlagen of the foot, cephalic hood, collar, hyponome (funnel), and the foot‐derived epidermal covers. We suggest that extensions of the collar‐funnel compartment and free epidermal folds derived from multiple topological foot regions may play an important role in forming the head complex, which is thought to be an important feature during the body plan transition. J. Morphol., 2008. © 2007 Wiley‐Liss, Inc.
Can principal component analysis provide atmospheric circulation or teleconnection patterns?
Authors: Compagnucci Rosa H. , Richman Michael B. 
Published: July 2007

AbstractThis investigation examines principal component (PC) methodology and the interpretation of the displays, such as eigenvalue magnitude, loadings and scores, which the methodology provides. The key question posed is, to what extent can S‐ and T‐mode decompositions of a dispersion matrix yield the kinds of interpretations placed on them typically? In particular, a series of experiments are designed based on various amalgamations of three distinct synoptic flow patterns. Since these flow patterns are known, a priori, this allows testing via subtle alterations of the methodology to determine whether there is equivalence between the S‐ and T‐mode decompositions, the degree to which the flow patterns or teleconnections can be recovered by each mode, and the interpretation of each mode.The findings are examined in two contexts: how well they classify the flow patterns, and how well they provide meaningful teleconnections. Both correlation and covariance dispersion matrices are used to determine differences that arise from the standardization. Additionally, unrotated and rotated results are included. By examining a variety of commonly applied methodologies, the results hold for a wider range of studies. Key findings are that eigenvalue degeneracy can influence one mode (but not the other) or both modes for any set of flow patterns resulting in pattern intermixing at times. Similarly, such degeneracy is found in one or both dispersion matrices. Congruence coefficients are used to provide a measure of validity by matching the PC loadings to the parent correlations and covariances. This matching is vital as the loadings exhibit dipoles that have been interpreted historically as physically meaningful, but the present work indicates they may arise purely through the methodology. Overall, we observe that S‐mode results can be interpreted as teleconnection patterns and T‐mode as flow patterns for well‐designed analyses that are meticulously scrutinized for methodological problems. Copyright © 2007 Royal Meteorological Society
Strategy to improve the reproducibility of colloidal SERS
Authors: Tantra Ratna , Brown Richard J. C. , Milton Martin J. T. 
Published: July 2007

AbstractThere is a pressing need to improve the reproducibility of surface enhanced Raman spectroscopy (SERS) measurements, if the technique is to be used routinely for trace analysis. This is particularly true for colloidal SERS, in which data reproducibility is dominated by the final shape and size of metal clusters produced during colloid aggregation. This study presents general guidelines for designing appropriate measurement strategies that can be used to identify and optimise crucial steps in a protocol that leads to better reproducibility of the results. We show that the data reproducibility can be improved by optimising vortexing time during colloid aggregation, which we attribute to the formation of more reproducible metal clusters under conditions of ‘forced convection’. The study also investigated the effects of different storage conditions on the data reproducibility of SERS during a 6‐month study period. Storage conditions did not significantly influence the SERS reproducibility. However, at the end of 6 months, colloids that were stored (in plastic containers) at room temperature showed a difference in their quality, as mirrored by their different opto‐physical properties. This was made apparent through the analysis of UV‐vis spectroscopy measurements by principal component analysis. Copyright © 2007 John Wiley & Sons, Ltd.
Procyanidins: extraction and micro‐ encapsulation
Authors: Zhang Lianfu , Mou Dehua , Du Yanshan 
Published: July 2007

AbstractAs by‐products of grape juice and wine production, grape seeds are a rich source of procyanidins but are usually discarded as waste. We have treated grape seeds with supercritical fluid extraction to remove the oils and have extracted the procyanidins from the residues. In order to extend the shelf life, micro‐encapsulating methods for procyanidins were studied: the use of gum arabic and maltodextrin as wall materials (the contents of arabic gum and maltodextrin were 40% and 60%, respectively). The raw materials were then mixed (the ratio of core substance to wall material was 30:70 w/w and the content of the slurry was 20% w/v). After homogenisation, spray drying was used to prepare microcapsules. The micro‐encapsulation efficiency was up to 88.84%. Analysis of the product showed that the procyanidin was not changed during the processing and the procyanidin microcapsule membrane was uninterrupted and with fairly good integrity. The stability of the products was also obviously improved. Copyright © 2007 Society of Chemical Industry