bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alterations in the oligodendrocyte lineage, myelin, and white matter in adult mice lacking the chemokine receptor CXCR2
Authors: Padovani‐Claudio Dolly A. , Liu Liping , Ransohoff Richard M. , Miller Robert H. 
Published: August 2006

AbstractOligodendrocyte precursor cell (OPC) proliferation and migration are critical for the development of myelin in the central nervous system (CNS). Previous studies showed that localized expression of the chemokine CXCL1 signals through the receptor CXCR2 to inhibit the migration and enhance the proliferation of spinal cord OPCs during development. Here, we report structural and functional alterations in the adult CNS of Cxcr2−/− mice. In Cxcr2−/− adult mice, we observed regional alterations in the density of oligodendrocyte lineage cells in Cxcr2−/− adult mice, with decreases in the cortex and anterior commissure but increases in the corpus callosum and spinal cord. An increase in the density and arborization of spinal cord NG2 positive cells was also observed in Cxcr2−/− adult mice. Compared with wild‐type (WT) littermates, Cxcr2−/− mice exhibited a significant decrease in spinal cord white matter area, reduced thickness of myelin sheaths, and a slowing in the rate of central conduction of spinally elicited evoked potentials without significant changes in axonal caliber or number. Biochemical analyses showed decreased levels of myelin basic protein (MBP), proteolipid protein (PLP), and glial fibrillary acidic protein (GFAP). In vitro studies showed reduced numbers of differentiated oligodendrocytes in Cxcr2−/− spinal cord cultures. Together, these findings indicate that the chemokine receptor CXCR2 is important for the development and maintenance of the oligodendrocyte lineage, myelination, and white matter in the vertebrate CNS. © 2006 Wiley‐Liss, Inc.
Role of N‐cadherin in Schwann cell precursors of growing nerves
Authors: Wanner Ina B. , Guerra Nicole K. , Mahoney James , Kumar Aman , Wood Patrick M. , Mirsky Rhona , Jessen Kristján R. 
Published: August 2006

AbstractIn the present paper, we determine the localization and developmental regulation of N‐cadherin in embryonic rat nerves and examine the role of N‐cadherin in this system. We also identify a major transition in the architecture of embryonic nerves and relating it to N‐cadherin expression. We find that in early embryonic nerves, N‐cadherin is primarily expressed in Schwann cell precursors. Pronounced expression is seen at distal nerve fronts where these cells associate with growth cones, and the proximal nerve ends, in boundary cap cells. Unexpectedly, N‐cadherin is downregulated as precursors generate Schwann cells, coinciding with the time at which most axons make target connections. Therefore, glial N‐cadherin expression is essentially restricted to the period of axon outgrowth. We also provide evidence that N‐cadherin supports the formation of contacts between Schwann cell precursors and show that these cells are a favorable substrate for axon growth, unlike N‐cadherin‐negative Schwann cells. Induction of N‐cadherin expression in Schwann cells by neuregulin‐1 restores their ability to form contacts and support axon growth. Finally, we show that the loss of glial N‐cadherin during embryonic nerve development is accompanied by a transformation of nerve architecture, involving the appearance of endoneurial connective tissue space, fibroblasts, Schwann cell basal lamina, and blood vessels. Because N‐cadherin is likely to promote the extensive glial contacts typical of the compact embryonic nerve, we suggest that N‐cadherin loss at the time of Schwann cell generation allows endoneurial space to appear between the glial cells, a development that eventually permits the extensive interactions between connective tissue and individual axon–Schwann cell units necessary for myelination. © 2006 Wiley‐Liss, Inc.
The developmental expression of K+ channels in retinal glial cells is associated with a decrease of osmotic cell swelling
Authors: Wurm Antje , Pannicke Thomas , Iandiev Ianors , Wiedemann Peter , Reichenbach Andreas , Bringmann Andreas 
Published: August 2006

AbstractA major function of glial cells is the control of osmotic and ionic homeostasis, mediated by K+ and water movements predominantly through inwardly rectifying K+ (Kir) and aquaporin water channels. It has been suggested that K+ currents through Kir channels are implicated in the regulation of glial cell volume. Here, we investigated whether the developmental increase in Kir channel expression in Müller glial cells of the rat retina is associated with an alteration of cell volume regulation under anisoosmotic conditions. Around the time of eye opening at postnatal day (P) 15, developing retinal glial cells fully alter the profile of their membrane conductances, from a current pattern with prominent fast transient K+ and Na+ currents to a pattern of noninactivating currents through Kir and delayed rectifier K+ channels. Concomitantly, aquaporins‐1 and ‐4 are expressed in the developing retina. This is accompanied by a conspicuous alteration of the swelling characteristics of cells; somata of immature glial cells in early postnatal retinas (P5–P15) swell under hypotonic stress but no swelling is inducible in mature cells at P18 and thereafter. However, glial cells at all developmental stages swell when their Kir channels are blocked by Ba2+. The postnatal maturation of Kir channel currents and volume regulation in retinal glial cells is delayed by visual deprivation. The data suggest that Kir channels are crucially involved in osmotic volume homeostasis of mature glial cells, and that the absence of Kir channels in immature cells is a major cause of their insufficient volume regulation. © 2006 Wiley‐Liss, Inc.
Differential effects of agarose and poly(lactic‐co‐glycolic acid) on dendritic cell maturation
Authors: Yoshida Mutsumi , Babensee Julia E. 
Published: August 2006

AbstractApplication of biomaterials in combination products in which the biomaterial is presented to the host with a biological component prompts the need for understanding the biomaterial‐associated adjuvant effect in the immune response against antigens associated with such a product. We have previously demonstrated that a polymer commonly used in tissue engineering and vaccine delivery, poly(lactic‐co‐glycolic acid) (PLGA), exerts an adjuvant effect in vivo, which was supported by PLGA‐induced dendritic cell (DC) maturation in vitro. In this study, the effects of agarose and PLGA on DC maturation were compared in vitro to establish differential biomaterial effects. Human monocyte‐derived DCs were treated with agarose or PLGA microparticles or films, and their maturation effect was measured as expression of costimulatory and MHC class II molecules, allostimulatory capacity, and proinflammatory cytokine secretion. Direct comparison of DC maturation phenotype indicated that PLGA was a stronger stimulus of DC maturation than agarose, and this maturation was not affected by microparticle phagocytosis. However, agarose‐treated DCs showed higher activation of nuclear factor κB (NFκB) 24 h after the initial stimulation of DCs. Taken together, these results demonstrate differential biomaterial effects on DC maturation, substantiating the maturation effect of PLGA, and provide screening methods for biomaterial adjuvant effect for applications in combination products. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Biomimetic artificial ECMs stimulate bone regeneration
Authors: Chung Eugene H. , Gilbert Michele , Virdi Amarjit S. , Sena Kotaro , Sumner Dale R. , Healy Kevin E. 
Published: August 2006

AbstractWe demonstrate that a biomimetic polymer network is capable of affecting bone regeneration in vivo. Starting with a foundation consisting of an environmentally responsive poly(N‐isopropylacrylamide‐co‐acrylic acid) hydrogel, we incorporated matrix metalloproteinase‐13 (MMP‐13) degradable crosslinkers and peptides containing integrin‐binding domains (i.e., Arg‐Gly‐Asp) to create a biomimetic matrix designed to encourage osteoblast migration and proliferation. We independently tuned matrix stiffness and peptide concentration to generate a response surface model of osteoblast proliferation on different types of matrices. Osteoblast proliferation was significantly influenced by matrix stiffness (i.e., its complex modulus) and peptide concentration. When implanted in a rat femoral ablation model, these matrices induced bone regeneration only when protease degradable crosslinks were used to create the network. For the matrices with MMP‐13 degradable crosslinkers, the bone formed had a trabecular‐like structure and was distributed throughout the marrow space. Based on the correlated effects of matrix stiffness and ligand concentration, the response surface model will facilitate improvements in the regenerative capacity of these artificial extracellular matrices. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Gelatin–tricalcium phosphate membranes immobilized with NGF, BDNF, or IGF‐1 for peripheral nerve repair: An in vitro and in vivo study
Authors: Chen Ming‐Hong , Chen Pei‐Ru , Chen Mei‐Hsiu , Hsieh Sung‐Tsang , Lin Feng‐Huei 
Published: August 2006

AbstractIn the present study, NGF, BNDF from the neurotrophin family and IGF‐1 were covalently immobilized on gelatin–tricalcium phosphate (GTG) membrane using carbodiimide. We investigated the effects of these growth factors released from the GTG composites on cultured PC12 cells and sciatic nerve regeneration across a 10‐mm‐long gap in rats. In PC12 cell culture, the total protein content and MTT assay indicated more cell attachment on the composites modified with growth factors. The IGF‐1 group showed a higher survival promotion effect on PC12 cells than did BDNF and NGF groups. On the other hand, NGF released from the composite showed the highest level of neuritogenesis for PC12 cells in neurite outgrowth assay. In the animal study, the GTG conduits modified with various growth factors were well tolerated by the host tissue. In the regenerated nerves, the number of the axons per unit area of the BDNF group was significantly higher than that of NGF and GTG groups but similar to that of IGF‐1 group. However, the average axon size was the largest in NGF group. This result was in concordance with the neurite outgrowth assay in which NGF showed the highest neuritogenic potential. In the assessment of motor and sensory recovery after nerve repair, conduits modified with various neurotrophic factors showed a more favorable outcome in compound muscle action potential. The BDNF group had a better gastrocnemic muscle weight ratio than blank GTG repair. Nevertheless, the different effects of GTG conduits modified with various neurotrophic factors on functional recovery cannot be simply illustrated in the sciatic function index. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Low‐intensity ultrasound stimulates the viability and matrix gene expression of human articular chondrocytes in alginate bead culture
Authors: Choi Byung Hyune , Woo Jeong‐Im , Min Byoung‐Hyun , Park So Ra 
Published: August 2006

AbstractWe investigated the effects of low‐intensity ultrasound (LIUS) on the activity of human articular chondrocytes isolated from osteoarthritis patients and cultured in the three‐dimensional alginate beads. LIUS was treated at 0, 100, 200, and 300 mW/cm2 for 10 min everyday for 2, 7, or 15 days. LIUS induced the viability of cells only at day 15 but not until day 7 after treatment, when examined by trypan blue exclusion and LIVE/DEAD® assay kit. When examined at day 7, the proliferation of cells was not changed by LIUS in the 3H‐thymine incorporation. The expression of matrix producing proteins (type II collagen and proteoglycan) was clearly induced by 200–300 mW/cm2 LIUS in the incorporation of radioactivity and Northern blot analysis. Although the expression of MMP‐1, a matrix degrading protein, was decreased, that of TIMP‐1, an inhibitor of MMPs, was not affected by LIUS. Histological analysis revealed an increase in the number and size of glycosaminoglycan‐positive lacunae and cellular organelles, appearing as rough endoplasmic reticulum and mitochondria by LIUS. These results showed that the viability and metabolism of human articular chondrocytes in alginate culture was induced by LIUS treatment, suggesting that they could be a promising autologous source for cartilage tissue engineering. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Evaluation of chondrogenesis within PEGT: PBT scaffolds with high PEG content
Authors: Mahmood Tahir A. , Shastri V. Prasad , van Blitterswijk Clemens A. , Langer Robert , Riesle Jens 
Published: August 2006

AbstractPorous poly(ethylene glycol) terephthalate:poly (butylene terephthalate) (PEGT:PBT) scaffolds with high PEG molecular weight (1000 g/mole) and PEGT content (60%) were fabricated using two different processes—paraffin templating and compression molding—for cartilage engineering applications. This polymer composition has previously been shown to enable chondrocyte adhesion and maintain differentiated phenotype in 2D monolayer culture. The influence of 3D polymer scaffold processing on the formation of cartilaginous tissue was studied by seeding primary immature bovine chondrocytes within cylindrical scaffolds in mixed flask reactors for 3 days, followed by cultivation in culture plates for a total of 10 or 24 days. Tissue–polymer constructs were evaluated morphologically by SEM and histology, and quantitatively for cellularity, total collagen, and glycosaminoglycan content, all of which remained statistically equivalent for each time point tested, irrespective of fabrication method. These data demonstrate that the polymers engineered for this study were able to support chondrogenesis independent of scaffold fabrication process, with the influence of pore architecture lessened by the highly hydrated scaffold microenvironments induced by high PEG content. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Application of the lithium and magnesium initiators for the synthesis of glycolide, lactide, and ϵ‐caprolactone copolymers biocompatible with brain tissue
Authors: Dobrzyński Piotr , Kasperczyk Janusz , Jelonek Katarzyna , Ryba Mirosław , Walski Michał , Bero Maciej 
Published: August 2006

AbstractThe subject of this work is new method of the synthesis of biodegradable copolymers compatible with brain tissue. Copolymerization of glycolide with lactide was conducted in solution or in bulk in the presence of LiBu, LiAcac, MgBu2, Mg(acac)2 as initiators. In all cases, copolymers with molecular weight of 20000–40000 were obtained, which enables to use them as drug carriers. During the reactions of copolymer chain growth, the intermolecular transesterification occurs, changing the distribution of comonomeric units in copolymer chain. Magnesium initiators showed a lower contribution to transesterification in comparison with lithium and calcium compounds. The copolymerization of glycolide with ε‐caprolactone using magnesium compounds as initiators was also described. The random glycolide/ε‐caprolactone copolymer (10/90) obtained with MgBu2 was used in in vivo study in the forms of microspheres and foils. Complete degradation of microspheres during 6 weeks was observed after the implantation to brain tissue. All implanted copolymers are compatible with brain tissue. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Bacteriostatic polymer film immobilization
Authors: El‐Hayek Rami F. , Dye Kevin , Warner John C. 
Published: August 2006

AbstractCoatings of quaternary ammonium tertiary structures (QUATS) copolymerized with 4‐vinylbenzylthymine (VBT) exhibited high antimicrobial activity against Escherichia coli. Immobilization of QUATS improves environmental performance by preventing release of antibacterials to the environment, helping to preclude the emergence of resistant strains. The crosslinking immobilization scheme reported herein provides a more environmentally benign and more inexpensive synthesis than previously reported, thus reducing the use of solvents, energy, and production time. Development of water soluble, thymine‐based photopolymers was inspired by the UV‐induced 2π + 2π photocyclodimerization of thymine in DNA. Copolymers of 4‐vinylbenzylthymine and trimethylammonium chloride, triethylammonium chloride, or dimethyloctylammonium chloride were synthesized in different monomer ratios. The antibacterial properties were tested by coating VBT:QUATS in sterilized petri dishes, crosslinking under short UV light, spraying with aqueous suspensions of bacterial cells, air drying, and then applying agar media to promote bacterial growth. The plates were incubated for 24 h at 37°C. The number of viable cells ranged from 17 to 0% growth. Immobilized VBT:QUAT copolymers are antiseptic surfaces that can be produced in an environmentally benign fashion. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Damage and recovery of the bone growth mechanism in young rats following 5‐fluorouracil acute chemotherapy
Authors: Xian Cory J. , Cool Johanna C. , Pyragius Tim , Foster Bruce K. 
Published: August 2006

AbstractChemotherapy‐induced bone growth arrest and osteoporosis are significant problems in paediatric cancer patients, and yet how chemotherapy affects bone growth remains unclear. This study characterised development and resolution of damage caused by acute chemotherapy with antimetabolite 5‐fluorouracil (5‐FU) in young rats in the growth plate cartilage and metaphyseal bone, two important tissues responsible for bone lengthening. In metaphysis, 5‐FU induced apoptosis among osteoblasts and preosteoblasts on days 1–2. In growth plate, chondrocyte apoptosis appeared on days 5–10. Interestingly, Bax was induced prior to apoptosis and Bcl‐2 was upregulated during recovery. 5‐FU also suppressed cell proliferation on days 1–2. While proliferation returned to normal by day 3 in metaphysis, it recovered partially on day 3, overshot on days 5–7 and normalised by day 10 in growth plate. Histologically, growth plate heights decreased by days 4–5 and returned normal by day 10. In metaphysis, primary spongiosa height was also reduced, mirroring changes in growth plate thickness. In metaphyseal secondary spongiosa, a reduced bone volume was observed on days 7–10 as there were fewer but more separated trabeculae. Starting from day 4, expression of some cartilage/bone matrix proteins and growth factors (TGF‐β1 and IGF‐I) was increased. By day 14, cellular activity, histological structure and gene expression had returned normal in both tissues. Therefore, 5‐FU chemotherapy affects bone growth directly by inducing apoptosis and inhibiting proliferation at growth plate cartilage and metaphyseal bone; after the acute damage, bone growth mechanism can recover, which is associated with upregulated expression of matrix proteins and growth factors. J. Cell. Biochem. 99: 1688–1704, 2006. © 2006 Wiley‐Liss, Inc.
Molecular and immunohistochemical analyses of cardiac troponin T during cardiac development in the Mexican axolotl, Ambystoma mexicanum
Authors: Zhang C. , Pietras K.M. , Sferrazza G.F. , Jia P. , Athauda G. , Rueda‐de‐Leon E. , Maier J.A. , Dube D.K. , Lemanski S.L. , Lemanski L.F. 
Published: August 2006

AbstractThe Mexican axolotl, Ambystoma mexicanum, is an excellent animal model for studying heart development because it carries a naturally occurring recessive genetic mutation, designated gene c, for cardiac nonfunction. The double recessive mutants (c/c) fail to form organized myofibrils in the cardiac myoblasts resulting in hearts that fail to beat. Tropomyosin expression patterns have been studied in detail and show dramatically decreased expression in the hearts of homozygous mutant embryos. Because of the direct interaction between tropomyosin and troponin T (TnT), and the crucial functions of TnT in the regulation of striated muscle contraction, we have expanded our studies on this animal model to characterize the expression of the TnT gene in cardiac muscle throughout normal axolotl development as well as in mutant axolotls. In addition, we have succeeded in cloning the full‐length cardiac troponin T (cTnT) cDNA from axolotl hearts. Confocal microscopy has shown a substantial, but reduced, expression of TnT protein in the mutant hearts when compared to normal during embryonic development. J. Cell. Biochem. 100: 1–15, 2007. © 2006 Wiley‐Liss, Inc.
Mouse translation elongation factor eEF1A‐2 interacts with Prdx‐I to protect cells against apoptotic death induced by oxidative stress
Authors: Chang Ruying , Wang Eugenia 
Published: August 2006

AbstracteEF1A‐1 and eEF1A‐2 are two isoforms of translation elongation factor eEF1A. In adult mammalian tissues, isoform eEF1A‐1 is present in all tissues except neurons, cardiomyocytes, and myotubes, where its isoform, eEF1A‐2, is the only form expressed. Both forms of eEF1A have been characterized to function in the protein elongation step of translation, and eEF1A‐1 is shown to possess additional non‐canonical roles in actin binding/bundling, microtubule bundling/severing, and cellular transformation processes. To study whether eEF1A‐2 has similar non‐canonical functions, we carried out a yeast two‐hybrid screening using a full sequence of mouse eEF1A‐2 as bait. A total of 78 hits, representing 23 proteins, were identified and validated to be true positives. We have focused on the protein with the highest frequency of hits, peroxiredoxin I (Prdx‐I), for in‐depth study of its functional implication for eEF1A‐2. Here we show that Prdx‐I coimmunoprecipitates with eEF1A‐2 from extracts of both cultured cells and mouse tissues expressing this protein, but it does not do so with its isoform, eEF1A‐1, even though the latter is abundantly present. We also report that an eEF1A‐2 and Prdx‐I double transfectant increases resistance to peroxide‐induced cell death as high as 1 mM peroxide treatment, significantly higher than do single transfectants with either gene alone; this protection is correlated with reduced activation of caspases 3 and 8, and with increased expression of pro‐survival factor Akt. Thus, our results suggest that eEF1A‐2 interacts with Prdx‐I to functionally provide cells with extraordinary resistance to oxidative stress‐induced cell death. J. Cell. Biochem. 100: 267–278, 2007. © 2006 Wiley‐Liss, Inc.
Phosphatidic acid regulates the affinity of the murine phosphatidylinositol 4‐phosphate 5‐kinase‐Iβ for phosphatidylinositol‐4‐phosphate
Authors: Jarquin‐Pardo Marta , Fitzpatrick Abbie , Galiano Floyd J. , First Eric A. , Davis J. Nathan 
Published: August 2006

AbstractType I phosphatidylinositol 4‐phosphate 5‐kinase (PI4P5K) catalyzes the phosphorylation of phosphatidylinositol 4 phosphate [PI(4)P] at carbon 5, producing phosphatidylinositol 4,5 bisphosphate [PI(4,5)P2]. Phosphatidic acid (PA) activates PI4P5K in vitro and plays a central role in the activation of PIP5K pathways in vivo. This report demonstrates that actin fiber formation in murine fibroblasts involves PA activation of PIP5Ks and defines biochemical interactions between PA and the PIP5Ks. Inhibition of phospholipase D production of PA results in the loss of actin fibers. Overexpression of the beta isoform of the type I murine phosphatidylinositol 4‐phosphate 5‐kinase (mPIP5K‐Iβ) maintains actin fiber structure in the face of phospholipase D inhibition. PA activates mPIP5K‐Iβ by direct binding to mPIP5K‐Iβ through both electrostatic and hydrophobic interactions, with the fatty acid acyl chain length and degree of saturation acting as critical determinants of binding and activation. Furthermore, kinetic analysis suggests that phosphorylation of the PI(4)P substrate does not follow classical Michaelis–Menten kinetics. Instead, the kinetic data are consistent with a model in which mPIP5K‐Iβ initially binds to the lipid micelle and subsequently binds the PI(4)P substrate. In addition, the kinetics indicate substrate inhibition, suggesting that mPIP5K‐Iβ contains an inhibitory PI(4)P‐binding site. These results suggest a model in which mPIP5K‐Iβ is surrounded by PI(4)P, but is unable to catalyze its conversion to PI(4,5)P2 unless PA is bound. J. Cell. Biochem. 100: 112–128, 2007. © 2006 Wiley‐Liss, Inc.