bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tanshinone IIA from Salvia miltiorrhiza BUNGE inhibits human aortic smooth muscle cell migration and MMP‐9 activity through AKT signaling pathway
Authors: Jin Un‐Ho , Suh Seok‐Jong , Chang Hyen Wook , Son Jong‐Keun , Lee Seung Ho , Son Kun‐Ho , Chang Young‐Chae , Kim Cheorl‐Ho 
Published: November 2007

AbstractSmooth muscle cell (SMC) migration plays an important role in normal angiogenesis and is relevant to disease‐related vascular remodeling in conditions such as brain arteriovenous malformations, pulmonary hypertension, arteriosclerosis, and restenosis after angioplasty. In this present study, we showed that tanshinone IIA, the major lipid‐soluble pharmacological constituent of Salvia miltiorrhiza BUNGE, inhibits human aortic smooth muscle cell (HASMC) migration and MMP‐9 activity. Tanshinone IIA significantly inhibited IκBα phosphorylation and p65 nuclear translocation through inhibition of AKT phosphorylation. Tanshinone IIA inhibited TNF‐α‐induced ERK and c‐jun phosphorylation, but not other MAPKs such as JNK and p38. Tanshinone IIA also inhibited NF‐κB and AP‐1 DNA‐binding. Moreover, tanshinone IIA inhibited the migration of TNF‐α‐induced HASMCs. Our results provide evidence that tanshinone IIA has multiple effects in the inhibition of HASMC migration and may offer a therapeutic approach to block HASMC migration. J. Cell. Biochem. 104: 15–26, 2008. © 2007 Wiley‐Liss, Inc.
Gravitational unloading induces an anti‐angiogenic phenotype in human microvascular endothelial cells
Authors: Mariotti Massimo , Maier Jeanette A.M. 
Published: November 2007

AbstractCreating conditions similar to those occurring during exposure of cells to microgravity modulates endothelial functions. We have previously demonstrated that human macrovascular endothelial cells in simulated hypogravity proliferate faster than controls, partly because they downregulate interleukin 1α. On the contrary, murine microvascular endothelial cells are growth inhibited in simulated hypogravity, and this is due, at least in part, to the decrease of interleukin 6. Since endothelial cells are very heterogeneous and differences between various species have been reported, we exposed human microvascular cells to gravitational unloading and found that it retards cell growth without affecting cell migration. Interestingly, we detected the induction of Tissue Inhibitor of Metalloprotease‐2, which inhibits endothelial growth in vitro and angiogenesis in vivo. Together with the finding that hypogravity stimulates the synthesis of nitric oxide, involved also in neovascularization, our results underscore a modulation of the angiogenic properties of microvascular human endothelial cells. We also show that hypogravity inhibits proteasome activity, thus suggesting that post‐translational mechanisms are involved in the adaptations of these cells to hypogravity. These results underscore that hypogravity differently impacts on micro‐ and macro‐vascular human endothelial cells. In particular, these results may shed some light on the molecular mechanisms contributing to the impairment of angiogenesis observed in different models in space. Our data might also explain why bioengineered tissues to be used for regenerative medicine fail to neovascularize when assembled in simulated hypogravity. J. Cell. Biochem. 104: 129–135, 2008. © 2007 Wiley‐Liss, Inc.
N‐Glycosylation affects the adhesive function of E‐Cadherin through modifying the composition of adherens junctions (AJs) in human breast carcinoma cell line MDA‐MB‐435
Authors: Zhao Hongbo , Liang Yulong , Xu Zhibin , Wang Liying , Zhou Feng , Li Zengxia , Jin Jiawei , Yang Yong , Fang Zhengyu , Hu Yali , Zhang Lineng , Su Jianmin , Zha Xiliang 
Published: November 2007

AbstractE‐cadherin mediates calcium‐dependent cell–cell adhesion between epithelial cells. The ectodomain of human E‐cadherin contains four potential N‐glycosylation sites at Asn residues 554, 566, 618, and 633. In this study, the role of N‐glycosylation in E‐cadherin‐mediated cell–cell adhesion was investigated by site‐directed mutagenesis. In MDA‐MB‐435 cells, all four potential N‐glycosylation sites of human E‐cadherin were N‐glycosylated. Removal of N‐glycan at Asn‐633 dramatically affected E‐cadherin stability. In contrast, mutant E‐cadherin lacking the other three N‐glycans showed similar protein stability in comparison with wild‐type E‐cadherin. Moreover, N‐glycans at Asn‐554 and Asn‐566 were found to affect E‐cadherin‐mediated calcium‐dependent cell–cell adhesion, and removal of either of the two N‐glycans caused a significant decrease in calcium‐dependent cell–cell adhesion accompanied with elevated cell migration. Analysis of the composition of adherens junctions (AJs) revealed that removal of N‐glycans on E‐cadherin resulted in elevated tyrosine phosphorylation level of β‐catenin and reduced β‐ and α‐catenins at AJs. These findings demonstrate that N‐glycosylation may affect the adhesive function of E‐cadherin through modifying the composition of AJs. J. Cell. Biochem. 104: 162–175, 2008. © 2007 Wiley‐Liss, Inc.
Conversion of immortal liver progenitor cells into pancreatic endocrine progenitor cells by persistent expression of Pdx‐1
Authors: Jin Cai‐Xia , Li Wen‐Lin , Xu Fang , Geng Zhen H. , He Zhi‐Ying , Su Juan , Tao Xin‐Rong , Ding Xiao‐Yan , Wang Xin , Hu Yi‐Ping 
Published: November 2007

AbstractThe conversion of expandable liver progenitor cells into pancreatic beta cells would provide a renewable cell source for diabetes cell therapy. Previously, we reported the establishment of liver epithelial progenitor cells (LEPCs). In this work, LEPCs were modified into EGFP/Pdx‐1 LEPCs, cells with stable expression of both Pdx‐1 and EGFP. Unlike previous work, with persistent expression of Pdx‐1, EGFP/Pdx‐1 LEPCs acquired the phenotype of pancreatic endocrine progenitor cells rather than giving rise to insulin‐producing cells directly. EGFP/Pdx‐1 LEPCs proliferated vigorously and expressed the crucial transcription factors involved in beta cell development, including Ngn3, NeuroD, Nkx2.2, Nkx6.1, Pax4, Pax6, Isl1, MafA and endogenous Pdx‐1, but did not secrete insulin. When cultured in high glucose/low serum medium supplemented with cytokines, EGFP/Pdx‐1 LEPCs stopped proliferating and gave rise to functional beta cells without any evidence of exocrine or other islet cell lineage differentiation. When transplanted into diabetic SCID mice, EGFP/Pdx‐1 LEPCs ameliorated hyperglycemia by secreting insulin in a glucose regulated manner. Considering the limited availability of beta cells, we propose that our experiments will provide a framework for utilizing the immortal liver progenitor cells as a renewable cell source for the generation of functional pancreatic beta cells. J. Cell. Biochem. 104: 224–236, 2008. © 2007 Wiley‐Liss, Inc.
Internal energy distribution of peptides in electrospray ionization : ESI and collision‐induced dissociation spectra calculation
Authors: Pak Alireza , Lesage Denis , Gimbert Yves , Vékey Károly , Tabet Jean‐Claude 
Published: November 2007

AbstractThe internal energy of ions and the timescale play fundamental roles in mass spectrometry. The main objective of this study is to estimate and compare the internal energy distributions of different ions (different nature, degree of freedom ‘DOF’ and fragmentations) produced in an electrospray source (ESI) of a triple‐quadrupole instrument (Quattro I Micromass). These measurements were performed using both the Survival Yield method (as proposed by De Pauw) and the MassKinetics software (kinetic model introduced by Vékey). The internal energy calibration is the preliminary step for ESI and collision‐induced dissociation (CID) spectra calculation. meta‐Methyl‐benzylpyridinium ion and four protonated peptides (YGGFL, LDIFSDF, LDIFSDFR and RLDIFSDF) were produced using an electrospray source. These ions were used as thermometer probe compounds. Cone voltages (Vc) were linearly correlated with the mean internal energy values (<Eint >) carried by desolvated ions. These mean internal energy values seem to be slightly dependent on the size of the studied ion. ESI mass spectra and CID spectra were then simulated using the MassKinetics software to propose an empirical equation for the mean internal energy (<Eint >) versus cone voltage (Vc) for different source temperatures (T): < Eint > = [405 × 10−6 − 480 × 10−9 (DOF)] VcT + Etherm(T). In this equation, the Etherm(T) parameter is the mean internal energy due to the source temperature at 0 Vc. Copyright © 2007 John Wiley & Sons, Ltd.
Structural characterizations of lipids A by MS/MS of doubly charged ions on a hybrid linear ion trap/orbitrap mass spectrometer
Authors: Silipo Alba , De Castro Cristina , Lanzetta Rosa , Molinaro Antonio , Parrilli Michelangelo , Vago Giorgio , Sturiale Luisa , Messina Angela , Garozzo Domenico 
Published: November 2007

AbstractHere, a new ‘one pot’ and fast approach is described, based on electrospray ionization (ESI) of negative ions by using a hybrid linear ion trap/orbitrap mass spectrometer (LTQ/orbitrap) for MS and MS/MS analysis. By this method the distribution of the primary and secondary acyl residues of the intact lipid A is inferred by analysis of the ESI spectra measured in positive and negative mode. The analysis of these data allows an unequivocal assignment of the fatty acid distribution. This methodology was successfully tested on two different lipid A with known structures, deriving from the Agrobacterium tumefaciens and Escherichia coli lipopolysaccharides (LPS). Copyright © 2007 John Wiley & Sons, Ltd.
A flow injection electrospray ionization tandem mass spectrometric method for the simultaneous measurement of trimethylamine and trimethylamine N‐oxide in urine
Authors: Johnson David W. 
Published: November 2007

AbstractKey metabolites for the diagnosis of the genetic disorder trimethylaminuria are trimethylamine (TMA) and trimethylamine N‐oxide (TMAO). A rapid, automatable flow injection ESI‐MS/MS method for their measurement in urine has been developed. The TMA was derivatized with ethyl bromoacetate to form ethyl betaine bromide. The 2 min ESI‐MS/MS analysis employed four multiple reaction monitoring (MRM) ion pairs for derivatized TMA (146.1, 118.1), derivatized 2H9‐TMA (155.1, 127.1), TMAO (76.1, 58.1) and 2H9‐TMAO (85.1, 66.1). In control urine samples (n = 27) referred for suspected metabolic problems TMA was 0.11–1.19 mmol/mol creatinine, TMAO was 13.5–181 mmol/mol creatinine and the TMA/TMAO ratio was 0.0025–0.055. In five patients with diagnosed trimethylaminuria, TMA was 5.3–230 mmol/mol creatinine, TMAO was 0.36–607 mmol/mol creatinine and the TMA/TMAO ratio was 0.20–134. Copyright © 2007 John Wiley & Sons, Ltd.
Neural progenitor cells transplanted into the uninjured brain undergo targeted migration after stroke onset
Authors: Guzman Raphael , Bliss Tonya , De Los Angeles Alejandro , Moseley Mike , Palmer Theo , Steinberg Gary 
Published: November 2007

AbstractEndogenous neural stem cells normally reside in their niche, the subventricular zone, in the uninjured rodent brain. Upon stroke, these cells become more proliferative and migrate away from the subventricular zone into the surrounding parenchyma. It is not known whether this stroke‐induced behavior is due to changes in the niche or introduction of attractive cues in the infarct zone, or both. A related question is how transplanted neural stem cells respond to subsequent insults, including whether exogenous stem cells have the plasticity to respond to subsequent injuries after engraftment. We addressed this issue by transplanting neural progenitor cells (NPCs) into the uninjured brain and then subjecting the animal to stroke. We were able to follow the transplanted NPCs in vivo by labeling them with superparamagnetic iron oxide particles and imaging them via high‐resolution magnetic resonance imaging (MRI) during engraftment and subsequent to stroke. We find that transplanted NPCs that are latent can be activated in response to stroke and exhibit directional migration into the parenchyma, similar to endogenous neural NPCs, without a niche environment. © 2007 Wiley‐Liss, Inc.
Induction and subcellular localization of high‐mobility group box–1 (HMGB1) in the postischemic rat brain
Authors: Kim Jung‐Bin , Lim Chae‐Moon , Yu Young‐Mi , Lee Ja‐Kyeong 
Published: November 2007

AbstractHigh‐mobility group box–1 (HMGB1) was originally identified as a ubiquitously expressed, abundant nonhistone DNA‐binding protein. Recently, it was found to act as a cytokine‐like mediator of delayed endotoxin lethality and of acute lung injury. Previously, we reported that HMGB1 is massively released extracellularly and plays a cytokine‐like function in the postischemic brain. In the present study, we examined the expression profile and cellular distribution of HMGB1 in rat brain after transient focal cerebral ischemia. The expression of HMGB1 in infarction areas in the ipsilateral sides gradually declined over 2 days after 1 hr of middle cerebral artery occlusion (MCAO) to below the basal level. However, after 3 days of reperfusion, HMGB1 level increased to above the basal level, especially in infarction cores, and this delayed induction was then maintained for several days. Immunohistochemistry using a polyclonal antibody against HMGB1 revealed its detailed expression pattern and subcellular localization in the postischemic brain. HMGB1 was found to be widely expressed throughout the normal brain and to be localized to the nuclei of almost all neurons and oligodendrocyte‐like cells. After 1 hr of MCAO, HMGB1 immediately translocated from the neuron nuclei to the cytoplasm and subsequently was depleted from neurons during the excitotoxicity‐induced acute damaging process. Moreover, beginning 2 days after reperfusion, HMGB1 was notably induced in activated microglia, astrocytes, and in microvascular structures, and these delayed gradual inductions were sustained for several days. These findings suggest that HMGB1 functions as a cytokine‐like mediator in a paracrine and autocrine manner in the postischemic brain. © 2007 Wiley‐Liss, Inc.
Sorting signals and regulation of cognate basolateral trafficking in myelin biogenesis
Authors: Klunder Bert , Baron Wia , Schrage Cobi , de Jonge Jenny , de Vries Hans , Hoekstra Dick 
Published: November 2007

AbstractA detailed understanding of trafficking pathways in mature oligodendrocytes is essential for addressing issues aimed at controlling (re)myelination by modulating myelin‐directed transport. Previously, we have shown that viral marker proteins HA and VSV G, on reaching the apical and basolateral surfaces of polarized epithelial cells, respectively, are primarily transported to the plasma membrane and myelin sheet, respectively, in oligodendrocytes (OLGs). In the present study, we demonstrated that in OLGs basolateral sorting signals similar to those in epithelial cells may target proteins to the myelin sheet, emphasizing the basolateral‐ and apical‐like nature of the myelin sheet and plasma membrane, respectively. Thus, substitution of essential amino acids reverses the direction of targeting of these proteins, whereas elimination of apical targeting of HA coincides with its dissipation from detergent‐resistant microdomains. Furthermore, protein kinase C activation negatively regulated transport of the OLG resident transmembrane protein PLP to the myelin sheet, like that of VSV G as shown previously, but did not affect the localization of the membrane‐associated myelin‐specific proteins MBP and CNP. These data imply that several distinctly regulated pathways operate in myelin sheet directed–transport that at least partly rely on a cognate basolateral sorting signal. © 2007 Wiley‐Liss, Inc.
Nicotinic acetylcholine receptor‐subunit mRNAs in the mouse superior cervical ganglion are regulated by development but not by deletion of distinct subunit genes
Authors: Putz G. , Kristufek D. , Orr‐Urtreger A. , Changeux J.‐P. , Huck S. , Scholze P. 
Published: November 2007

AbstractMice with deletions of nicotinic ACh receptor (nAChR) subunit genes are valuable models for studying nAChR functions. We could previously show in the mouse superior cervical ganglion (SCG) that the absence of distinct subunits affects the functional properties of receptors. Here, we have addressed the question of whether deletions of the subunits α5, α7, or β2 are compensated at the mRNA level, monitored by reverse transcription and quantitative real‐time polymerase chain reaction. Relative to our reference gene, α3, which is expressed in all SCG nAChRs, mRNA levels of β4 showed little change from birth until adult ages in intact ganglia of wild‐type mice. In contrast, α4 declined sharply after birth and was barely detectable in adult animals. α5, α7, and β2 subunit message levels also declined, though more slowly and less completely than α4. The subunits α6 and β3 were detected by conventional polymerase chain reaction at very low levels, if at all, whereas α2 was never seen in any of our samples. The developmental profile of nAChR mRNA levels in the three knockout strains did not differ markedly from that of wild‐type mice. Likewise, message levels of nAChR subunits were similar in cultures prepared from either wild‐type or knockout animals. Our observations indicate a developmental regulation of nAChR subunit mRNAs in the SCG of mice after birth that was not affected by the three knockouts under investigation. © 2007 Wiley‐Liss, Inc.
Neuregulin‐1 induces acetylcholine receptor transcription in the absence of GABPα phosphorylation
Authors: Herndon Carter A. , Fromm Larry 
Published: November 2007

AbstractLocalization of acetylcholine receptors (AChRs) to the postsynaptic region of muscle is mediated in part by transcriptional mechanisms, because the genes encoding AChR subunits are transcribed selectively in synaptic myofiber nuclei. Neuregulin‐1 (NRG‐1) is a synaptic signal and induces transcription of AChRs in muscle cells. Signaling by NRG‐1 is thought to involve the transcription factor GA‐binding protein (GABP), a heterodimer of GABPα, which is a member of the Ets family, and GABPβ. Phosphorylation of certain other Ets proteins outside the Ets DNA‐binding domain serves to stimulate transcriptional activation in response to extracellular signals. According to previous studies, NRG‐1 stimulates phosphorylation of GABPα at threonine 280 in the N‐terminal region adjacent to the Ets domain, suggesting that GABPα phosphorylation might contribute to NRG‐1 responsiveness. To determine the functional importance of the N‐terminal region of GABPα and whether its function is regulated by phosphorylation, we generated muscle cell lines in which the endogenous GABPα gene was deleted and replaced by variants of GABPα mutated in the N‐terminal region. We found that NRG‐1 can induce transcription in cells with mutated T280 phosphorylation site, indicating that T280 phosphorylation does not contribute to NRG‐1 responsiveness. We also found that NRG‐1‐induced transcription occurs in cells missing the entire N‐terminal region of GABPα. Because NRG‐1 signaling is not expected to alter the function of the C‐terminal region, which remains in these cells, these results suggest that GABPβ, or other interacting components, rather than GABPα directly, is targeted by NRG‐1 signaling. © 2007 Wiley‐Liss, Inc.
Reduction of wear volume from ultrahigh molecular weight polyethylene knee components by the addition of vitamin E
Authors: Teramura Satoshi , Sakoda Hideyuki , Terao Tomohiro , Endo Miguel M. , Fujiwara Kunihiko , Tomita Naohide 
Published: November 2007

AbstractWear performance and debris‐size distribution of vitamin E (DL‐α tocopherol, VE)‐added ultrahigh molecular weight polyethylene (UHMWPE) was evaluated using a knee‐simulator test. VE was mixed with GUR 1050 UHMWPE powder at 0.3 wt%, and the tibial components of the knee joint were made by direct compression molding. The VE‐added UHMWPE showed consistently lower wear volume throughout the test. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:460–464, 2008
Stimulation of nitric oxide mechanotransduction in single osteoblasts using atomic force microscopy
Authors: McGarry James G. , Maguire Paula , Campbell Veronica A. , O'Connell Brian C. , Prendergast Patrick J. , Jarvis Suzanne P. 
Published: November 2007

AbstractNitric oxide (NO) released from mechanosensitive bone cells plays a key role in the adaptation of bone structure to its mechanical usage. Despite its importance in bone, the mechanisms involved in NO mechanotransduction at the cellular level remain unknown. Using combined atomic force microscopy and fluorescence microscopy, we report both stimulation and real‐time monitoring of NO responses in single osteoblasts induced by application of quantified periodic indenting forces to the osteoblast membrane. Peak forces ranging from 17 to 50 nN stimulated three distinct NO responses in the indented osteoblasts: (1) a rapid and sustained diffusion of NO from the perinuclear region, (2) diffusion of NO from localized pools throughout the osteoblast, and (3) an initial increase and subsequent drop in intracellular NO. Force‐indentation characteristics showed considerable interosteoblast variation in elasticity. NO responses were associated with application of force to more rigid membrane sites, suggesting cytoskeletal involvement in mechanotransduction. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:513–521, 2008
Effects of different molecular weight hyaluronan products on the expression of urokinase plasminogen activator and inhibitor and gelatinases during the early stage of osteoarthritis
Authors: Hsieh Yih‐Shou , Yang Shun‐Fa , Lue Ko‐Huang , Chu Shu‐Chen , Lu Ko‐Hsiu 
Published: November 2007

AbstractHyaluronan or hyaluronic acid (HA) has been used to treat osteoarthritic knees for more than 30 years. Here, we tested the hypothesis that HA with high molecular weight (MW) would have greater effects than HA with low MW on the expression of the plasminogen activator (PA)/plasmin system and gelatinases [matrix metalloproteinase (MMP)‐2 and MMP‐9] during early development of osteoarthritis (OA). We compared the levels of MMP‐2, MMP‐9, urokinase‐type PA (u‐PA), and PA inhibitor‐1 (PAI‐1) in a series of chondral, meniscal, and synovial cultures of early OA after treatment with or without three different MW HA products (Hyalgan and Artz with low MW, and Synvisc with high MW). Gelatin zymography revealed that three different HA products could decrease the secretion of MMP‐2 in all tissue cultures and MMP‐9 in meniscal and synovial cultures time‐dependently. Enzyme‐linked immunosorbent assay showed that Artz and Synvisc had significant inhibition on u‐PA and PAI‐1 levels after 24 h, but Hyalgan did at 96 h. Compared with Hyalgan and Artz, Synvisc provided the greatest ability to inhibit MMP‐2, MMP‐9, u‐PA, and PAI‐1 expression. Our studies clearly demonstrate that the therapeutic effects of using HA to treat early OA may be partially dependant on downregulation of the PA/plasmin system and gelatinases expression, which delay the structural progression of the disease. HA with high MW might have a greater ability than that with low MW to offer effective protection for articular cartilage. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:475–484, 2008