Relevant bibliographies by topics / Versican

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Versican'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Versican"

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Papadas, Athanasios, Garrett Arauz, Alexander Cicala, Joshua Wiesner, and Fotis Asimakopoulos. "Versican and Versican-matrikines in Cancer Progression, Inflammation, and Immunity." Journal of Histochemistry & Cytochemistry 68, no. 12 (July 6, 2020): 871–85. http://dx.doi.org/10.1369/0022155420937098.

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Versican is an extracellular matrix proteoglycan with key roles in multiple facets of cancer development, ranging from proliferative signaling, evasion of growth-suppressor pathways, regulation of cell death, promotion of neoangiogenesis, and tissue invasion and metastasis. Multiple lines of evidence implicate versican and its bioactive proteolytic fragments (matrikines) in the regulation of cancer inflammation and antitumor immune responses. The understanding of the dynamics of versican deposition/accumulation and its proteolytic turnover holds potential for the development of novel immune biomarkers as well as approaches to reset the immune thermostat of tumors, thus promoting efficacy of modern immunotherapies. This article summarizes work from several laboratories, including ours, on the role of this central matrix proteoglycan in tumor progression as well as tumor-immune cell cross-talk:
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Brune, Jourdan E., Mary Y. Chang, William A. Altemeier, and Charles W. Frevert. "Type I Interferon Signaling Increases Versican Expression and Synthesis in Lung Stromal Cells During Influenza Infection." Journal of Histochemistry & Cytochemistry 69, no. 11 (October 19, 2021): 691–709. http://dx.doi.org/10.1369/00221554211054447.

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Versican, a chondroitin sulfate proteoglycan, is an essential component of the extracellular matrix (ECM) in inflammatory lung disease. Versican’s potential as an immunomodulatory molecule makes it a promising therapeutic target for controlling host immune responses in the lungs. To establish changes to versican expression and accumulation during influenza A viral pneumonia, we document the temporal and spatial changes to versican mRNA and protein in concert with pulmonary inflammatory cell infiltration. These studies were performed in the lungs of wild-type C57BL6/J mice on days 3, 6, 9, and 12 post-infection with influenza A virus using immunohistochemistry, in situ hybridization, and quantitative digital pathology. Using duplex in situ hybridization, we demonstrate that type I interferon signaling contributes significantly to versican expression in lung stromal cells. Our findings show that versican is a type I interferon–stimulated gene in pulmonary fibroblasts and pericytes in the context of viral pneumonia. These data also provide a guide for future studies to determine the role of versican in the pulmonary immune response to influenza infection:
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Rahmani, Maziar, Brian W. Wong, Lisa Ang, Caroline C. Cheung, Jon M. Carthy, Hubert Walinski, and Bruce M. McManus. "Versican: signaling to transcriptional control pathwaysThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigator's Forum." Canadian Journal of Physiology and Pharmacology 84, no. 1 (January 2006): 77–92. http://dx.doi.org/10.1139/y05-154.

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Versican, a chondroitin sulfate proteoglycan, is one of the main components of the extracellular matrix, which provides a loose and hydrated matrix during key events in development and disease. Versican participates in cell adhesion, proliferation, migration, and angiogenesis, and hence plays a central role in tissue morphogenesis and maintenance. In addition, versican contributes to the development of a number of pathologic processes including atherosclerotic vascular diseases, cancer, tendon remodeling, hair follicle cycling, central nervous system injury, and neurite outgrowth. Versican is a complex molecule consisting of modular core protein domains and glycosaminoglycan side chains, and there are various steps of synthesis and processes regulating them. Also, there is differential temporal and spatial expression of versican by multiple cell types and in different developmental and pathological time frames. To fully appreciate the functional roles of versican as it relates to changing patterns of expression in development and disease, an in depth knowledge of versican’s biosynthetic processing is necessary. The goal of this review is to evaluate the current status of our knowledge regarding the transcriptional control of versican gene regulation. We will be focusing on the signal transduction pathways, promoter regions, cis-acting elements, and trans-factors that have been characterized.
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Sheng, Wang, Guizhi Wang, David P. La Pierre, Jianping Wen, Zhaoqun Deng, Chung-Kwun Amy Wong, Daniel Y. Lee, and Burton B. Yang. "Versican Mediates Mesenchymal-Epithelial Transition." Molecular Biology of the Cell 17, no. 4 (April 2006): 2009–20. http://dx.doi.org/10.1091/mbc.e05-10-0951.

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Versican is a large extracellular chondroitin sulfate proteoglycan that belongs to the family of lecticans. Alternative splicing of versican generates at least four isoforms named V0, V1, V2, and V3. We show here that ectopic expression of versican V1 isoform induced mesenchymal-epithelial transition (MET) in NIH3T3 fibroblasts, and inhibition of endogenous versican expression abolished the MET in metanephric mesenchyme. MET in NIH3T3 cells was demonstrated by morphological changes and dramatic alterations in both membrane and cytoskeleton architecture. Molecular analysis showed that V1 promoted a “switch” in cadherin expression from N- to E-cadherin, resulting in epithelial specific adhesion junctions. V1 expression reduced vimentin levels and induced expression of occludin, an epithelial-specific marker, resulting in polarization of V1-transfected cells. Furthermore, an MSP (methylation-specific PCR) assay showed that N-cadherin expression was suppressed through methylation of its DNA promoter. Exogenous expression of N-cadherin in V1-transfected cells reversed V1's effect on cell aggregation. Reduction of E-cadherin expression by Snail transfection and siRNA targeting E-cadherin abolished V1-induced morphological alteration. Transfection of an siRNA construct targeting versican also reversed the changed morphology induced by V1 expression. Silencing of endogenous versican prevented MET of metanephric mesenchyme. Taken together, our results demonstrate the involvement of versican in MET: expression of versican is sufficient to induce MET in NIH3T3 fibroblasts and reduction of versican expression decreased MET in metanephric mesenchyme.
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Zimmermann, DR, MT Dours-Zimmermann, M. Schubert, and L. Bruckner-Tuderman. "Versican is expressed in the proliferating zone in the epidermis and in association with the elastic network of the dermis." Journal of Cell Biology 124, no. 5 (March 1, 1994): 817–25. http://dx.doi.org/10.1083/jcb.124.5.817.

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The expression of the large chondroitin sulfate proteoglycan versican was studied in human adult skin. For this purpose, bacterial fusion proteins containing unique portions of the versican core protein were prepared. Polyclonal antibodies against the fusion proteins specifically reacted with versican from a proteoglycan fraction of MG63 osteosarcoma cells. In immunohistochemical experiments, the affinity-purified antibodies localized versican in the stratum basale of the epidermis, as well as in the papillary and reticular layers of the dermis. An apparent codistribution of versican with the various fiber forms of the elastic network of the dermis suggested an association of versican with microfibrils. Both dermal fibroblasts and keratinocytes expressed versican in culture during active cell proliferation. In line with the observation that versican is absent in the suprabasal layers of the epidermis where keratinocytes terminally differentiate, culture conditions promoting keratinocyte differentiation induced a down-regulation of versican synthesis. In Northern blots versican mRNA could be detected in extracts from proliferating keratinocytes and dermal fibroblasts. Comparison of RNA preparations from semi-confluent and confluent fibroblast cultures demonstrated decreasing amounts of versican mRNA at higher cell densities. This inverse correlation of versican expression and cell density was confirmed by indirect immunofluorescence staining of cultured fibroblasts and keratinocytes. The localization of versican in the basal zone of the epidermis as well as the density dependence of versican in cell cultures suggest a general function of versican in cell proliferation processes that may not solely be confined to the skin.
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Landolt, R. M., L. Vaughan, K. H. Winterhalter, and D. R. Zimmermann. "Versican is selectively expressed in embryonic tissues that act as barriers to neural crest cell migration and axon outgrowth." Development 121, no. 8 (August 1, 1995): 2303–12. http://dx.doi.org/10.1242/dev.121.8.2303.

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Chondroitin sulfate proteoglycans have been implicated in the regulation of cell migration and pattern formation in the developing peripheral nervous system. To identify whether the large aggregating proteoglycan versican might be mediating these processes, we prepared monospecific antibodies against a recombinant core protein fragment of chick versican. The purified antibodies recognize the predominant versican splice-variants V0 and V1. Using these antibodies, we revealed a close correlation between the spacio-temporal expression of versican and the formation of molecular boundaries flanking or transiently blocking the migration pathways of neural crest cells or motor and sensory axons. Versican is present in the caudal sclerotome, the early dorsolateral tissue underneath the ectoderm, the pelvic girdle precursor and to a certain extent in the perinotochordal mesenchyme. Versican is completely absent from tissues invaded by neural crest cells and extending axons. Upon completion of neural crest cell migration and axon outgrowth, versican expression is shifted to pre-chondrogenic areas. Since versican inhibits cellular interactions with fibronectin, laminin and collagen I in vitro, the selective expression of versican within barrier tissues may be linked to a functional role of versican in the guidance of migratory neural crest cells and outgrowing axons.
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Mohamed, Mohamed. "Versican and coronary artery spasm." Medical Research Journal 11, no. 1 (June 2012): 1–6. http://dx.doi.org/10.1097/01.mjx.0000414711.94482.58.

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Theocharis, Achilleas D. "Versican in Health and Disease." Connective Tissue Research 49, no. 3-4 (January 2008): 230–34. http://dx.doi.org/10.1080/03008200802147571.

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Kenagy, Richard D., Anna H. Plaas, and Thomas N. Wight. "Versican Degradation and Vascular Disease." Trends in Cardiovascular Medicine 16, no. 6 (August 2006): 209–15. http://dx.doi.org/10.1016/j.tcm.2006.03.011.

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LeBaron, R. G., D. R. Zimmermann, and E. Ruoslahti. "Hyaluronate binding properties of versican." Journal of Biological Chemistry 267, no. 14 (May 1992): 10003–10. http://dx.doi.org/10.1016/s0021-9258(19)50191-0.

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Dissertations / Theses on the topic "Versican"

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Rahmani, Maziar. "Regulation of the versican gene : implications for vascular health and disease." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/368.

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Versican, a chondroitin sulfate proteoglycan, is one of the main components of the extracellular matrix and hence plays a central role in tissue morphogenesis and a number of pathologic processes. My main goal has been to investigate the mechanisms of versican gene regulation, focusing on the signal transduction pathways, promoter regions, cis-acting elements,and trans- factors. This thesis puts forth new knowledge regarding transcriptional regulation of the human versican gene. In chapter III, I present the cloning of a 752-bp fragment of the human versican promoter (- 634/+118 bp) and nine stepwise 5' deletion fragments in the PGL3-luciferase reporter plasmid. Furthermore, I identify three potential enhancer and two repressor regions in this promoter. I also demonstrate that both cAMP and C/EBPf3 enhanced and repressed versican transcription in HeLa cells and rat aortic smooth muscle cells (SMC),respectively, suggesting that versican transcription is differentially regulated by the respective mediator and transcription factor in epithelial cells and SMC. In chapter IV, I reveal the role ofPI3K/PKB/GSK-30 signaling pathway in regulating versican promoter activity and transcription. Furthermore, I identify that the 0-catenin/TCF-4 transcription factor complex, one of the downstream targets of GSK-3[3, mediates versican promoter activity and transcription. In chapter V, I identify that variations in C-terminal regions of TCF family members determine the irrepressor or enhancer properties on Wnt target genes. Furthermore, I show that curcumin is a strong inhibitor of the P-catenin/TCF-p300 mediated gene expression. In chapter VI, I demonstrate that the androgen receptor trans-activates versican transcription in prostate cancer cells. Furthermore, I show cross-talk between the androgen receptor and 13-catenin in regulating versican transcription in prostate stromal fibroblasts. Overall, this study charts previously uncharacterized promoter elements, transcription factors, and signal transduction pathways involved in regulation of the versican gene.
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Tani, Hirohiko. "Role of Versican in the Pathogenesis of Peritoneal Endometriosis." Kyoto University, 2017. http://hdl.handle.net/2433/227588.

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Maurice, Sean Bertram. "Metalloproteinase cleavage of versican at the fibroblast cell surface." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/14410.

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Versican is a large aggregating proteoglycan expressed in the pericellular matrix of fibroblast cells. It is highly expressed during development and remodeling. The regulated synthesis and degradation of versican are associated with physiological remodeling. Versican is expressed in fibroproliferative lesions of human pulmonary fibrosis and atherosclerosis. Stromal expression of versican is associated with many forms of cancer and may be predictive of poor prognosis. Abnormal persistence of the versican-rich matrix may contribute to fibroproliferative and oncogenic processes. The process of versican degradation is not understood, but as versican is a pericellular molecule, physiological degradation likely involves cell surface-associated proteolysis. As such, the overarching hypothesis for this work is that regulated versican turnover involves the cell surface-associated metalloproteinases ADAMTS-2, MMP-2 and MT1-MMP, that are expressed in versican-rich remodeling lesions. ADAMTS-2 is a procollagen N-propeptidase involved in collagen fibrillogenesis. As procollagen is synthesized in a versican-rich matrix, it was hypothesized that ADAMTS- 2 might bind and process versican. MMP-2 and MT1-MMP in complex with TIMP-2, are activated at the cell surface during wound healing, pulmonary fibrosis and cancer. Versican was purified from human fetal lung fibroblast cultures for in vitro proteolysis experiments. The purified versican preparation was characterized by electrophoresis, chromatography, spectrophotometry and mass spectrometry. ADAMTS-2 and versican localization in normal and fibrotic human lungs were investigated. ADAMTS-2 was shown to co-purify with versican from human fetal lung fibroblasts. Bovine ADAMTS-2 was purified from fetal calf skin and shown to cleave purified human versican. The plant lectin concanavalin-A (ConA) induces a matrix degradative phenotype and is used here to investigate the process of versican degradation relative to apoptotic iii events in human fetal lung fibroblast cultures. Con-A induced increased expression of MMP-2 and MT1-MMP in human fetal lung fibroblasts and a concomitant loss of versican from the matrix. Microarray analysis was used to investigate expression of possible versican-degrading enzymes and their inhibitors, expressed in response to ConA. Recombinant MMP-2 and MT1-MMP were shown to process purified versican in vitro. This work expands upon the body of knowledge of versican turnover and should help in the search for therapeutic avenues to treat fibroproliferative and oncogenic processes.
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Fielder, Helen Louise. "Structural and Functional Characterisation of the G1 Domain from Human Versican." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491447.

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Versican, a chondroitin sulfate proteoglycan, fomis large extracellular link proteinstabilised complexes with hyaluronan (HA), thought to confer structural properties such as elasticity of blood vessels. HA binding is mediated through the N-terminal 01 domain of versican (VOl), which is composed of an Ig domain and two contiguous Link modules. In addition to the Link modules, the Ig domain may be required for HA .binding, perhaps stabilising the overall fold of the 01 domain. There is currently no high-resolution structure available for VOl, or for Type C HA-binding domains (HABO), which are comprised ofa pair of Link modules. Previously, VO I from human versican was expressed in Drosophila S2 cells as two N-glycoforms (dVOI); it was shown to interact with HA and this was unaffected by deglycosylation (Seyfried et aI., 2005b). Initial crystallisation attempts were limited by low expression yields (-0.5 mg/litre) and perhaps glycosylation. Here, VOl has - therefore been expressed a) in E. coli (eVGl) and b) in an unglycosylated form in Drosophila S2 cells in the presence of tunicamycin (tVO I), to generate material more suitable for structural studies. eVG1 was refolded by rapid dilution and, after ion exchange chromatography, 7-9 mg/litre pure protein was obtained. eVGl and tVOl have similar HA-binding properties to dVGl, but intrinsic fluorescence analysis indicated that only eVO1 was correctly folded. Glycosylation may therefore be required for correct folding of VG1 in eukaryotic systems. eVG1 also interacts with the TSO-6 Link module (as previously demonstrated for dVG1 (Kuznetsova et aI., 2006)). These functional studies, in combination with information from 10 NMR, ESI-TOF-MS and dynamic light scattering, indicated that eVGI was suitable for further biophysical/functional studies. eVG1 was screened against -1500 conditions, but an eVGI crystal was not obtained. Lack of success with crystallography may be due to a non-functional fraction of the eVOI preparation. Biotinylated-eVOI was found to be a useful tool for histological staining of HA in tissue sections. eVGI is also being used to raise a monoclonal antibody against the GI domain of versican and to investigate whether eVG1 can promote elastogenesis in vascular smooth muscle cells. Previously it has been hypothesised that VGI interacts with HA every HAlO and that this interaction displays all-or-nothing co-operativity (Seyfried et aI., 2006). By SECMALLS analysis it was found that eVOI 'footprints' a length of polymeric HA which is approximately double the length that was previously thought i.e. HAI8-22. Competition experiments using HA22 oligomers indicate that the interaction is positively co-operative, although further experiments need to be performed to ascertain whether the interaction shows all-or-nothing co-operativity. In sununary, a method of producing high yields of VOI has been developed and this material has facilitated structural, functional, cell biology and histology studies. Further characterisation of HA-VOI complex formation is improving our understanding of extracellular matrix organisation.
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Foulcer, Simon. "Structural and functional studies on the G1 domain of human versican." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/structural-and-functional-studies-on-the-g1-domain-of-human-versican(2670c4da-7050-4280-8a7c-fc02ab3e8bb3).html.

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The chondroitin sulphate proteoglycan (CSPG) versican forms complexes with hyaluronan (HA), which are essential in a range of functions including cellular proliferation and migration. Four isoforms of versican result from alternative splicing. Furthermore, biological roles have been identified for the proteolytic cleavage product of versican which contains the N-terminal G1 hyaluronan binding domain. All of these versican forms have different tightly regulated tissue expression profiles. Consequently, impaired regulation is associated with a number of disease pathologies. For example the largest variants (V0/V1) have been shown to be negative indicators of disease outcome in a number of malignant cancers and are a marker of disease progression in atherosclerosis. Interestingly, the smaller versican isoform V3 which lacks CS chains has been demonstrated to have the potential to reverse disease associated phenotypes. The motivation for carrying out the work in this thesis was to try and gain a better understanding of how versican functions on a molecular scale. In this regard, the first aim was to investigate the structure of the hyaluronan binding region of versican using a construct called VG1. The structure of VG1 was analysed in the presence and absence of hyaluronan oligomers. This revealed an insight into the multi-modular structure of the versican hyaluronan binding region and demonstrated that on binding to HA, VG1 under goes a conformational change. Furthermore, the interaction between VG1 and longer lengths of hyaluronan (pHA) was investigated. This demonstrated that when VG1 binds to pHA it is does so with positive cooperativity, packing very close to neighbouring VG1 molecules along a chain of HA. One consequence of this interaction was to reorganise pHA into a helical conformation, an organisation that was confirmed by a number of solution phase techniques. The effect of this reorganisation of pHA by VG1 on HA/CD44 interactions was also assessed. Previously the interaction between CD44 (a cell surface hyaluronan receptor) and long chains of HA (>30 kDa) was shown to be irreversible; however we demonstrate that VG1 can reverse this. Furthermore, a TSG-6 enhanced CD44/interaction was also completely reversed by the addition of VG1. This provides an indication that a functional hierarchy of hyaluronan binding proteins may exist which could have important implications in understanding the function of hyaluronan complexes. Currently, we do not know whether intact versican molecules could interact with HA in the same way as VG1. However, preliminary data suggests that the CS-containing variants (i.e. V0, V1 and V2) would not, whereas V3 and versican fragments could. This work provides an exciting mechanistic insight into the function of versican variants and their breakdown products.
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Kimata, Koji, Takayuki Miura, Hisashi Iwata, Tamayuki Shinomura, and Yoshihiro Nishida. "Abnormal occurrence of a large chondroitin sulfate proteoglycan, PG-M/versican in osteoarthritic cartilage." Thesis, Elsevier, 1994. http://hdl.handle.net/2237/16722.

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Pourmalek, Saloumeh. "Versican in the wound healing matrix : cellular interactions and degradation by matrix metalloproteinases." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/7098.

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In wound healing, versican is a component of the provisional matrix laid down at the site of injury by proliferating myofibroblasts. Versican interacts with a variety of matrix molecules and is believed to interact with the cell surface. The mechanism of interaction of versican with the cell surface, however, is not well documented. Return to normal tissue structure, at late stages of wound healing, involves degradation of versican and concomitant fibroblast apoptosis. Macrophage enzymes are candidates for versican degradation; however, the mechanisms of actions of these enzymes on versican and the rates and cleavage sites are not yet known. This thesis tests several hypotheses: 1) Versican interacts with cell surface receptors of myofibroblasts and macrophages; 2) Versican influences myofibroblast cell morphology during wound contraction; and 3) Macrophage matrix metalloproteinases degrade versican during wound resolution. We first attempted to identify macrophage and fibroblast versican-binding cell surface ligands. Using biotinylated constructs of the C-terminal domain of versican as baits, we identified versican and versican fragments as the main ligands for the C-terminal construct. However, we found that most versican could be released from the cell surface by hyaluronidase treatment, and concluded that versican is held at the fibroblast cell surface mainly through its interaction with hyaluronan. Next, we examined the influence of versican and hyaluronan on the physical properties of a collagenous matrix, and the cells embedded within the matrix, using a novel 3-dimensional collagen/versican/hyaluronan matrix model. We found that fibroblast cells in matrices containing versican express smooth muscle actin and take on a contractile morphology. Finally, we hypothesized that macrophage metalloproteinases degrade versican. The macrophage matrix metalloproteinases (MMPs), MMP 2, MMP-7, and MMP-12 were chosen as candidate enzymes, which we localized to the resolving phase of wound healing in the human lung. We found that MMP-7 and MMP-12 cleave versican at multiple sites in vitro, whereas MMP-2 cleaves versican at a limited number of sites. These macrophage enzymes may be important in clearing versican in vivo. A better understanding of the mechanism of versican degradation could enable therapeutic modification of the disease process in fibrosis, cancer, and nervous system regeneration.
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Carthy, Jonathon Morgan. "Cellular and molecular biology of Wnt signaling and versican expression in myofibroblast differentiation." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/39838.

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Wound healing is a complex and dynamic process that restores tissue integrity after injury, but also contributes pathologically to the development of fibrosis. Growing evidence suggests a role for Wnt signaling during normal and aberrant wound healing. The proteoglycan versican is a target of Wnt signaling that is expressed following injury and accumulates pathologically in many chronic inflammatory conditions. In this dissertation, I hypothesized that Wnt signaling and its target versican are key regulators of mesenchymal cell phenotype. In Aim 1, I demonstrated that treatment of cultured fibroblasts with Wnt3a, a canonical Wnt ligand, stimulates the formation of a myofibroblast-like phenotype characterized by increased expression of smooth muscle α-actin. These changes appear to be mediated by Wnt3a upregulating the expression of TGF-β and its associated signaling through SMAD2 in a β-catenin-dependent mechanism. In Aim 2, I show that Wnt3a alters the phenotype of vascular smooth muscle cells and stimulates the formation of a contractile and secretory phenotype in these cells that is associated with increased gap junction communication. Again, these changes occurred through a mechanism that was dependent on canonical Wnt signaling. In Aim 3, I explored the functional roles of versican by examining its expression following injury to cultures of valve myofibroblasts. My data indicate that versican is secreted as extracellular matrix following injury to valve cells, and suggests a role for the membrane receptor CD44 in organizing this provisional versican matrix. In Aim 4, I delved further into the functional roles of versican by expressing this proteoglycan in murine fibroblasts. In this aim I showed that versican expression promotes myofibroblast differentiation, and these changes appear to be mediated by activation of TGF-β signaling. Lastly, in Aim 5, I explored potential intracellular functions for versican, and provide evidence to suggest versican localizes to the nucleus in mesenchymal cells where it regulates the organization of the mitotic spindle during cell division. Collectively, these data suggest Wnt signaling and versican are key regulators of mesenchymal cell phenotype, and as such, are important mediators of a wound healing response.
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Sotoodehnejadnematalahi, Fattah. "Studies on regulation of versican gene expression by hypoxia in primary human macrophages." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/10304.

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Hypoxia is a hallmark of many pathological tissues. Macrophages accumulate in hypoxic sites and up-regulate a number of hypoxia-inducible genes. The extracellular matrix glycoprotein versican has recently been identified as one such gene, but the mechanisms responsible for hypoxic induction are not well characterised. Here, hypoxic up-regulation of versican was investigated in primary human monocyte-derived macrophages. Flow cytometry of isolated peripheral blood mononuclear cells demonstrated a three-fold increase in versican protein in macrophages after 5 days incubation in hypoxia. Subset analysis showed that macrophages, and not lymphocytes, are the main peripheral blood mononuclear cells which express, and show hypoxic up-regulation of, versican protein and mRNA. This study showed that versican mRNA is up-regulated 34-fold after exposure of primary human macrophages to hypoxia for 18hrs. Further investigation showed that versican mRNA decay rates are not affected by hypoxia, indicating that hypoxic induction of versican mRNA is mediated by increased promoter activity rather than increased mRNA stability. Extensive deletion and transfection analysis of proximal versican promoter luciferase reporter constructs identified two regions which are required for high level activity of the promoter in hypoxic primary human macrophages. A recent publication suggested that hypoxic induction of versican mRNA in macrophages is mediated by the hypoxia inducible transcription factor HIF-1α. Here, bacterial lipopolysaccharide and the hypoxia mimetic agents desferrioxamine and cobalt chloride, three stimuli which are known to induce HIF-1α, were used to investigate the role of HIF-1 in the up-regulation of versican mRNA. Neither LPS nor cobalt chloride caused up-regulation of versican mRNA, although control HIF-1 regulated genes were up-regulated, suggesting that high-level transcription of the versican promoter in hypoxia occurs via a HIF-1 independent mechanism. Lastly, two specific inhibitors of PI3-kinase, LY294002 and Wortmannin, were shown to down-regulate hypoxic induction of versican mRNA, suggesting a possible role for PI3-kinase.
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Miyazaki, Yumiko. "Versican V1 in human endometrial epithelial cells promotes BeWo spheroid adhesion in vitro." Kyoto University, 2019. http://hdl.handle.net/2433/242394.

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Books on the topic "Versican"

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Zondervan Publishing House (Grand Rapids, Mich.), ed. Nuevo Testamento: Nueva Versión Internacional = New Testament : New International Version. Grand Rapids, Mich: Zondervan Pub. House, 1991.

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Society, International Bible. Nuevo Testamento: Nueva Versión Internacional = New Testament : New International Version. Colorado Springs, CO: Sociedad Biblica Internacional, 1991.

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Pokémon: Ruby version, sapphire version. Roseville, CA: Prima Games, 2003.

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Geoffrey, Chaucer. A Spanish version of Chaucer's Troilus and Criseyde =: Versión española del Troilo y Criseida de Chaucer. Lewiston, N.Y: Edwin Mellen Press, 2008.

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Versión celeste. Madrid: Cátedra, 1989.

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John, Updike. Roger's version. New York: Knopf, 1986.

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John, Updike. Roger's version. London: Deutsch, 1986.

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Works, Book, ed. Cover version. London: Book Works, 2004.

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Apollonia, Francois d'. Version invisible. Longueuil, Québec: Le Préambule, 1987.

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Richler, Mordecai. Barney's version. New York: Vintage Books, 2010.

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Book chapters on the topic "Versican"

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Foulcer, Simon J., Anthony J. Day, and Suneel S. Apte. "Isolation and Purification of Versican and Analysis of Versican." In Methods in Molecular Biology, 559–78. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1398-6_43.

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Foulcer, Simon J., Anthony J. Day, and Suneel S. Apte. "Isolation and Purification of Versican and Analysis of Versican Proteolysis." In Methods in Molecular Biology, 587–604. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1714-3_46.

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Papadas, Athanasios, and Fotis Asimakopoulos. "Versican in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 55–72. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48457-6_4.

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Keire, Paul A., Inkyung Kang, and Thomas N. Wight. "Versican: Role in Cancer Tumorigenesis." In Extracellular Matrix in Tumor Biology, 51–74. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60907-2_4.

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Papadas, Athanasios, Alexander Cicala, Sean G. Kraus, Garrett Arauz, Alexander Tong, Dustin Deming, and Fotis Asimakopoulos. "Versican in Tumor Progression, Tumor–Host Interactions, and Cancer Immunotherapy." In The Extracellular Matrix and the Tumor Microenvironment, 93–118. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-99708-3_5.

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Rahmani, Maziar, Jon M. Carthy, and Bruce M. McManus. "Mapping of the Wnt/β-Catenin/TCF Response Elements in the Human Versican Promoter." In Methods in Molecular Biology, 35–52. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-498-8_3.

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Apte, Suneel S. "The Pivotal Role of Versican Turnover by ADAMTS Proteases in Mammalian Reproduction and Development." In Proteoglycans in Stem Cells, 35–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73453-4_3.

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Dours-Zimmermann, María T., and Dieter R. Zimmermann. "A Novel Strategy for a Splice-Variant Selective Gene Ablation: The Example of the Versican V0/V2 Knockout." In Methods in Molecular Biology, 63–85. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-498-8_5.

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Darnell, Roger. "My Version and Your Version." In The Communications Consultant's Foundation, 151–55. New York: Routledge, 2021. http://dx.doi.org/10.4324/9781003177951-20.

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Kretzmann, N., and G. Nuchelmans. "Another Version." In The Quarrel over Future Contingents (Louvain 1465–1475), 380–96. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1039-3_25.

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Conference papers on the topic "Versican"

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Bischel, Kristen Moriah, Philip Emmerich, Tonela Qyli, Stephanie McGregor, Mitchell Depke, Nathaniel Verhagen, Dustin Deming, et al. "Abstract 403: Versican proteolysis in endometrial cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-403.

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Babiarz, Christopher P., Philip B. Emmerich, Carley M. Sprackling, Cheri A. Pasch, Linda Clipson, Kristina A. Matkowskyj, Fotis Asimakopoulos, and Dustin A. Deming. "Abstract 4583: Versican accumulation and proteolysis in neuroendocrine tumors." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4583.

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Babiarz, Christopher P., Philip B. Emmerich, Carley M. Sprackling, Cheri A. Pasch, Linda Clipson, Kristina A. Matkowskyj, Fotis Asimakopoulos, and Dustin A. Deming. "Abstract 4583: Versican accumulation and proteolysis in neuroendocrine tumors." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4583.

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Pappas, Apostolos, Sofia Magkouta, Maria Vazakidou, and Ioannis Kalomenidis. "Role of tumor derived versican in experimental malignant pleural mesothelioma." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa496.

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Derin, M. E., I. Karadağ, A. C. Urhan, G. Toksoylu, G. Asan, M. Bayram, H. O. Doğan, M. Şahin, and A. Şahin. "AB1128 Evaluation of serum versican levels in patients with familial mediterranean fever (FMF)." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4022.

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Annoni, Raquel, Ligia Couceiro, Silvio Barbosa, Tatiana Lancas, Salvatore Battaglia, Marisa Dolhnikoff, Pieter Hiemstra, Peter Sterk, Klaus Rabe, and Thais Mauad. "Versican and collagen-III expression in bronchial and pulmonary muscular arteries in COPD patients." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2446.

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Wang, Gang, Masaru Suzuki, Marjan Luinge, John E. McDonough, Corry-Anke Brandsma, Mark Elliott, John V. Gosselink, et al. "Alteration In Decorin And Versican In The Lung Extra-Cellular Matrix In Centrilobular Emphysema." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6676.

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Setoguchi, Tomohiko, Hirotoshi Kikuchi, Ichirota Iino, Toshiki Kawabata, Masayoshi Yamamoto, Manabu Ohta, Kinji Kamiya, et al. "Abstract 805: Microarray analysis reveals Versican and CD9 as novel prognostic factors of GIST." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-805.

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Gupta, N., R. Kumar, R. Khan, T. Seth, B. Garg, and A. Sharma. "PO-284 Involvement of versican, a chondroitin sulfate proteolgycan in the pathogenesis of multiple myeloma." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.798.

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de Wit, Meike, Eric J. Belt, Pien M. Delis van Diemen, Beatriz Carvalho, Veerle M. Coupé, Hein B. Stockmann, Herman Bril, Jeroen A. Belien, Remond J. Fijneman, and Gerrit A. Meijer. "Abstract 4526: Lumican and Versican predict good outcome in stage II and III colon cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4526.

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Reports on the topic "Versican"

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Larsson, M., and P. G. Alm. GEODIM, Version 2.1: Users manual (English units version). Office of Scientific and Technical Information (OSTI), January 1991. http://dx.doi.org/10.2172/10195772.

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Bamberger, Judy, Timothy Coddington, Robert Firth, Daniel Klein, and Dave Stinchcomb. Version Description and Installation Guide Kernel Version 3.0. Fort Belvoir, VA: Defense Technical Information Center, December 1989. http://dx.doi.org/10.21236/ada219292.

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Poston, D. I., and H. R. Trellue. User`s manual, version 1.00 for Monteburns, version 3.01. Office of Scientific and Technical Information (OSTI), June 1998. http://dx.doi.org/10.2172/307942.

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Gray, Norman. An RDF version of the VO Registry Version 1.00. Edited by Norman Gray. International Virtual Observatory Alliance, September 2007. http://dx.doi.org/10.5479/ads/bib/2007ivoa.rept.0920g.

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Herton, Michael J. UT20-PCTE Browser Tool Version Description Document Version 0.1. Fort Belvoir, VA: Defense Technical Information Center, June 1992. http://dx.doi.org/10.21236/ada257429.

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Smith, Robert C., and Michael J. Horton. UT20-Ada PCTE Binding Version Description Document Version 0.1. Fort Belvoir, VA: Defense Technical Information Center, June 1992. http://dx.doi.org/10.21236/ada257430.

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Hilmer, Robert V., T. Hall, C. Roth, A. G. Ling, G. P. Ginet, and D. Madden. AF-Geospace User's Manual Version 2.5.1 and Version 2.51P. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada563130.

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Hilmer, R. V., G. Ginet, T. Hall, E. Holeman, and M. Tautz. AF-Geospace User's Manual Version 1.4 and Version 1.4P. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada387593.

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Rupert, J. Dec VAX version of MAGRAV, users guide version 2.1. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1987. http://dx.doi.org/10.4095/315282.

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Frye, R., D. Levi, S. Routhier, and B. Wijnen. Coexistence between Version 1, Version 2, and Version 3 of the Internet-standard Network Management Framework. RFC Editor, March 2000. http://dx.doi.org/10.17487/rfc2576.

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