Relevant bibliographies by topics / Connective Tissue Growth Factor ECM

Academic literature on the topic 'Connective Tissue Growth Factor ECM'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Connective Tissue Growth Factor ECM"

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Effendi, Wiwin Is, and Tatsuya Nagano. "Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge." International Journal of Molecular Sciences 23, no. 11 (May 28, 2022): 6064. http://dx.doi.org/10.3390/ijms23116064.

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CTGF is upregulated in patients with idiopathic pulmonary fibrosis (IPF), characterized by the deposition of a pathological extracellular matrix (ECM). Additionally, many omics studies confirmed that aberrant cellular senescence-associated mitochondria dysfunction and metabolic reprogramming had been identified in different IPF lung cells (alveolar epithelial cells, alveolar endothelial cells, fibroblasts, and macrophages). Here, we reviewed the role of the CTGF in IPF lung cells to mediate anomalous senescence-related metabolic mechanisms that support the fibrotic environment in IPF.
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Ramirez, Francesco, Lynn Y. Sakai, Harry C. Dietz, and Daniel B. Rifkin. "Fibrillin microfibrils: multipurpose extracellular networks in organismal physiology." Physiological Genomics 19, no. 2 (October 4, 2004): 151–54. http://dx.doi.org/10.1152/physiolgenomics.00092.2004.

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Organismal physiology depends significantly on the proper assembly of extracellular matrix (ECM) macroaggregates that impart structural integrity to the connective tissue. Recent genetic studies in mice have unraveled unsuspected new functions of architectural matrix components in regulating signaling events that modulate patterning, morphogenesis, and growth of several organ systems. As a result, a new paradigm has emerged whereby tissue-specific organization of the ECM dictates not only the physical properties of the connective tissue, but also the ability of the matrix to direct a broad spectrum of cellular activities through the regulation of growth factor signaling. These observations pave the way to novel therapeutic approaches aimed at counteracting the deleterious consequences of perturbations of connective tissue homeostasis.
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Albeiroti, Sami, Artin Soroosh, and Carol A. de la Motte. "Hyaluronan’s Role in Fibrosis: A Pathogenic Factor or a Passive Player?" BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/790203.

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Fibrosis is a debilitating condition that can lead to impairment of the affected organ’s function. Excessive deposition of extracellular matrix (ECM) molecules is characteristic of most fibrotic tissues. Fibroblasts activated by cytokines or growth factors differentiate into myofibroblasts that drive fibrosis by depositing ECM molecules, such as collagen, fibronectin, and connective tissue growth factor. Transforming growth factor-β(TGF-β) is one of the major profibrotic cytokines which promotes fibrosis by signaling abnormal ECM regulation. Hyaluronan (HA) is a major ECM glycosaminoglycan that is regulated by TGF-βand whose role in fibrosis is emerging. Aside from its role as a hydrating, space filling polymer, HA regulates different cellular functions and is known to have a role in wound healing and inflammation. Importantly, HA deposition is increased in multiple fibrotic diseases. In this review we highlight studies that link HA to fibrosis and discuss what is known about the role of HA, its receptors, and its anabolic and catabolic enzymes in different fibrotic diseases.
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Harlow, Christopher R., Angela C. Bradshaw, Michael T. Rae, Kirsty D. Shearer, and Stephen G. Hillier. "Oestrogen formation and connective tissue growth factor expression in rat granulosa cells." Journal of Endocrinology 192, no. 1 (January 2007): 41–52. http://dx.doi.org/10.1677/joe.1.06689.

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Ovarian follicular development involves continual remodelling of the extracellular matrix (ECM) forming the basement membrane and intercellular framework that support granulosa cell (GC) growth and differentiation. Insight into the molecular regulation of ovarian ECM remodelling is potentially translatable to tissue remodelling elsewhere in the body. We therefore studied the link between a gene marker of ECM remodelling (connective tissue growth factor (CTGF)) and oestrogen biosynthesis (cytochrome P450aromatase (P450arom)) in rat granulosa cells. To determine if a cause–effect interaction exists, we used semi-quantitative in situ hybridisation to analyse patterns of CTGF and P450arom mRNA expression and immunohistochemistry to detect CTGF protein localisation throughout follicular development, and tested the actions of CTGF on oestrogen biosynthesis and oestradiol on CTGF mRNA expression in isolated GC in vitro. CTGF mRNA levels in GC rose gradually through small preantral (SP) and small antral (SA) stages of development to a maximum (fivefold higher) in large antral (LA) follicles. In preovulatory (PO) follicles, the CTGF mRNA level fell to 30% of that in SP follicles. P450arom mRNA also increased (threefold in LA relative to SP) throughout antral development follicles, but in contrast to CTGF continued to increase (12-fold) in PO follicles. In the cumulus oophorus of PO follicles, the residual GC CTGF mRNA expression increased with proximity to the oocyte, being inversely related to P450arom. Elsewhere in the follicle wall, there was a mural-to-antral gradient of CTGF mRNA expression, again inversely related to P450arom. Immunohistochemistry showed CTGF protein localisation broadly followed mRNA expression during follicular development, although the protein was also present in the theca interna and ovarian surface epithelium. Gradients in CTGF expression across the cumulus oophorus and follicle wall were similar to those observed for mRNA with CTGF protein expression being greatest in proximity to the oocyte. Treatment of isolated GC from preantral and SA follicles with recombinant human CTGF (1–100 ng/ml) did not affect basal or FSH-stimulated GC aromatase activity. However, in the absence of FSH, oestradiol (10−7–10−5 M) stimulated CTGF mRNA expression up to twofold. Conversely, FSH (10 ng/ml) alone reduced CTGF mRNA expression by 40% and combined treatment with FSH and oestradiol further suppressed CTGF to 10% of the control value. The oestrogen receptor (ER) antagonist, ICI 182 780 blocked the stimulatory and inhibitory effects of oestradiol, suggesting a specific ER-mediated mode of action on CTGF. Therefore, CTGF gene expression in GC is under local control by oestrogen whose effect (positive or negative) is modulated by FSH. This helps explain why gene expression of CTGF and P450arom diverge in FSH-induced PO follicles and has implications for oestrogenic regulation of CTGF formation elsewhere in the body.
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Silver, Frederick H., Dale DeVore, and Lorraine M. Siperko. "Invited Review: Role of mechanophysiology in aging of ECM: effects of changes in mechanochemical transduction." Journal of Applied Physiology 95, no. 5 (November 2003): 2134–41. http://dx.doi.org/10.1152/japplphysiol.00429.2003.

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Mechanical forces play a role in the development and evolution of extracellular matrices (ECMs) found in connective tissue. Gravitational forces acting on mammalian tissues increase the net muscle forces required for movement of vertebrates. As body mass increases during development, musculoskeletal tissues and other ECMs are able to adapt their size to meet the increased mechanical requirements. However, the control mechanisms that allow for rapid growth in tissue size during development are altered during maturation and aging. The purpose of this mini-review is to examine the relationship between mechanical loading and cellular events that are associated with downregulation of mechanochemical transduction, which appears to contribute to aging of connective tissue. These changes result from decreases in growth factor and hormone levels, as well as decreased activation of the phosphorelay system that controls cell division, gene expression, and protein synthesis. Studies pertaining to the interactions among mechanical forces, growth factors, hormones, and their receptors will better define the relationship between mechanochemical transduction processes and cellular behavior in aging tissues.
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Chang, Patrick C., Janine M. Low-Marchelli, Ashkan Shahbandi, Daniel J. Goff, and Catriona Jamieson. "Connective Tissue Growth Factor Induces Anti-Apoptotic Factors in Chronic Myeloid Leukemia Stem Cells." Blood 124, no. 21 (December 6, 2014): 1785. http://dx.doi.org/10.1182/blood.v124.21.1785.1785.

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Abstract Chronic Myeloid Leukemia (CML) is a progressive hematopoietic malignancy where expression of the oncogenic fusion protein BCR-ABL1 in leukemia stem cells (LSCs) prevents the proper differentiation of myeloid progenitor populations, leading to accumulation of undifferentiated blasts. Current treatments target BCR-ABL1 with tyrosine kinase inhibitors (TKIs). Though effective if administered continuously, TKIs generally fail to eradicate the bone marrow niche-residing LSCs responsible for patient relapse or progression of CML to its terminal stage, Blast Crisis (BC), as evidenced by the high molecular relapse rate following TKI discontinuation. Previous studies performed by ourselves and others show that BC progenitors (CD34+CD38+Lin-) exhibit stem-like behaviors, such as quiescence, self-renewal, and induction of pro-survival gene expression through alternative splicing of BCL2 family members, and thus behave like LSCs. Notably, BC CML LSCs co-cultured on LSC (SL/M2) supportive stroma are resistant to TKIs compared to culturing the cells alone, indicating a role of the extracellular matrix (ECM) in promoting LSC survival. We performed RNA-seq and qRT-PCR of CD34+CD38+Lin- progenitor cells in CML patient samples and found a significant increase in CTGF (Connective Tissue Growth Factor) expression in BC CML versus chronic phase (CP). Interestingly, CTGF is an ECM protein that enhances cell adhesion and has been shown to predict therapeutic resistance in cancers, such as acute lymphoblastic leukemia (ALL). Lentiviral overexpression of CTGF in a CML cell line K562 and CD34+ CP CML patient samples caused proliferation and a decrease in apoptosis markers (cleaved caspase-3), as measured by FACS analysis. Moreover, qRT-PCR analysis of mRNA indicated an increase in pro-survival BCL2 family gene expression. These changes were not observed in normal CD34+ cord blood cells. Currently, lentiviral CTGF transduction of CP CML followed by transplantation into RAG2-/-gc-/- and NSG-S mice will be used to determine the effects of CTGF on LSC maintenance in vivo. In conclusion, CTGF promotes CML LSC survival in vitro and thus could be a key factor in BC transformation and TKI resistance. Disclosures Jamieson: J&J, Roche: Research Funding.
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Miyashita, Naoya, and Akira Saito. "Organ Specificity and Heterogeneity of Cancer-Associated Fibroblasts in Colorectal Cancer." International Journal of Molecular Sciences 22, no. 20 (October 11, 2021): 10973. http://dx.doi.org/10.3390/ijms222010973.

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Fibroblasts constitute a ubiquitous mesenchymal cell type and produce the extracellular matrix (ECM) of connective tissue, thereby providing the structural basis of various organs. Fibroblasts display differential transcriptional patterns unique to the organ of their origin and they can be activated by common stimuli such as transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF) signaling. Cancer-associated fibroblasts (CAFs) reside in the cancer tissue and contribute to cancer progression by influencing cancer cell growth, invasion, angiogenesis and tumor immunity. CAFs impact on the tumor microenvironment by remodeling the ECM and secreting soluble factors such as chemokines and growth factors. Differential expression patterns of molecular markers suggest heterogeneous features of CAFs in terms of their function, pathogenic role and cellular origin. Recent studies elucidated the bimodal action of CAFs on cancer progression and suggest a subgroup of CAFs with tumor-suppressive effects. This review attempts to describe cellular features of colorectal CAFs with an emphasis on their heterogeneity and functional diversity.
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Vogelmann, R., D. Ruf, M. Wagner, G. Adler, and A. Menke. "Effects of fibrogenic mediators on the development of pancreatic fibrosis in a TGF-β1 transgenic mouse model." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 1 (January 1, 2001): G164—G172. http://dx.doi.org/10.1152/ajpgi.2001.280.1.g164.

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The pancreas morphology of transgenic mice that overexpress transforming growth factor-β1 (TGF-β1) in the pancreas resembles partially morphological features of chronic pancreatitis, such as progressive accumulation of extracellular matrix (ECM). Using this transgenic mouse model, we characterized the composition of pancreatic fibrosis and involved fibrogenic mediators. On day 14 after birth, fibrotic tissue was mainly composed of collagen type I and III. At this time, mRNA levels of TGF-β1 were increased. On day 70, the ECM composition was expanded by increased deposition of fibronectin, whereas connective tissue growth factor, fibroblast growth factor (FGF)-1, and FGF-2 mRNA expression levels were elevated in addition to TGF-β1. In parallel, the number of pancreatic stellate cells (PSC) increased over time. In vitro, TGF-β1 stimulated collagen type I expression but not fibronectin expression in PSC, in contrast to FGF-2, which stimulated both. This confirms that TGF-β1 mediates pancreatic fibrosis through activation of PSC and deposition of collagen type I and III at early time points. Furthermore, this points to an indirect mechanism in which TGF-β regulates pancreatic ECM assembly by induction of additional growth factors.
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Ritelli, Marco, Nicola Chiarelli, Valeria Cinquina, Nicoletta Zoppi, Valeria Bertini, Marina Venturini, and Marina Colombi. "RNA-Seq of Dermal Fibroblasts from Patients with Hypermobile Ehlers–Danlos Syndrome and Hypermobility Spectrum Disorders Supports Their Categorization as a Single Entity with Involvement of Extracellular Matrix Degrading and Proinflammatory Pathomechanisms." Cells 11, no. 24 (December 14, 2022): 4040. http://dx.doi.org/10.3390/cells11244040.

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Hypermobile Ehlers–Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD) are clinically overlapping connective tissue disorders of unknown etiology and without any validated diagnostic biomarker and specific therapies. Herein, we in-depth characterized the cellular phenotype and gene expression profile of hEDS and HSD dermal fibroblasts by immunofluorescence, amplicon-based RNA-seq, and qPCR. We demonstrated that both cell types show a common cellular trait, i.e., generalized extracellular matrix (ECM) disarray, myofibroblast differentiation, and dysregulated gene expression. Functional enrichment and pathway analyses clustered gene expression changes in different biological networks that are likely relevant for the disease pathophysiology. Specifically, the complex gene expression dysregulation (mainly involving growth factors, structural ECM components, ECM-modifying enzymes, cytoskeletal proteins, and different signal transducers), is expected to perturb many ECM-related processes including cell adhesion, migration, proliferation, and differentiation. Based on these findings, we propose a disease model in which an unbalanced ECM remodeling triggers a vicious cycle with a synergistic contribution of ECM degradation products and proinflammatory mediators leading to a functional impairment of different connective tissues reflecting the multisystemic presentation of hEDS/HSD patients. Our results offer many promising clues for translational research aimed to define molecular bases, diagnostic biomarkers, and specific therapies for these challenging connective tissue disorders.
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Pouw, Andrew E., Mark A. Greiner, Razek G. Coussa, Chunhua Jiao, Ian C. Han, Jessica M. Skeie, John H. Fingert, Robert F. Mullins, and Elliott H. Sohn. "Cell–Matrix Interactions in the Eye: From Cornea to Choroid." Cells 10, no. 3 (March 20, 2021): 687. http://dx.doi.org/10.3390/cells10030687.

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The extracellular matrix (ECM) plays a crucial role in all parts of the eye, from maintaining clarity and hydration of the cornea and vitreous to regulating angiogenesis, intraocular pressure maintenance, and vascular signaling. This review focuses on the interactions of the ECM for homeostasis of normal physiologic functions of the cornea, vitreous, retina, retinal pigment epithelium, Bruch’s membrane, and choroid as well as trabecular meshwork, optic nerve, conjunctiva and tenon’s layer as it relates to glaucoma. A variety of pathways and key factors related to ECM in the eye are discussed, including but not limited to those related to transforming growth factor-β, vascular endothelial growth factor, basic-fibroblastic growth factor, connective tissue growth factor, matrix metalloproteinases (including MMP-2 and MMP-9, and MMP-14), collagen IV, fibronectin, elastin, canonical signaling, integrins, and endothelial morphogenesis consistent of cellular activation-tubulogenesis and cellular differentiation-stabilization. Alterations contributing to disease states such as wound healing, diabetes-related complications, Fuchs endothelial corneal dystrophy, angiogenesis, fibrosis, age-related macular degeneration, retinal detachment, and posteriorly inserted vitreous base are also reviewed.
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Dissertations / Theses on the topic "Connective Tissue Growth Factor ECM"

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Tam, Y. Y. A. "Connective tissue growth factor in tissue fibrosis." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1448702/.

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Systemic Sclerosis (SSc) is a connective tissue disease characterised by inflammation and autoimmunity, vasculopathy, and interstitial remodelling and fibrosis. This thesis focuses on CTGF (CCN2), a member of the CCN family of matricellular proteins, as elevated CTGF expression is a hallmark of chronic fibrotic diseases such as SSc. In addition to the association of CTGF expression and fibrosis in human disease, experimentally, fibroblast-specific overexpression of CTGF has been shown to induce a fibrotic phenotype, as demonstrated in the Col1a2-CTGF transgenic mice. Prominent features of fibrosis included a thickened dermis, as well as excess collagen deposition in the skin and lung. This CTGF overexpression also provoked changes in the alveolar epithelium. In the lung of Col1a2-CTGF mice, immunostaining revealed a marked increase in the number of cells co-expressing the epithelial marker, TTF-1 and mesenchymal cell markers α-SMA and Snai1, indicative of epithelial-to-mesenchymal transition (EMT)-like changes. This suggested a role for the paracrine effects of CTGF in promoting the phenotypic switching of alveolar epithelial cells. EMT is likely to contribute, at least in part, to the accumulation of interstitial fibroblasts during fibrosis. Complementary in vitro studies in alveolar epithelial cells (AECs) showed that CTGF knockdown using siRNA suppressed TGF-β-induced mesenchymal cell proteins while inducing redistribution of the epithelial cell marker E-cadherin. Immunostaining and Western blotting showed that recombinant CTGF induced EMT-like morphological changes and expression of α-SMA in AECs. Finally, we were interested in whether the reduction or absence of CTGF could abrogate fibrosis. Knockdown of CTGF suppressed the induction of fibrotic proteins in TGF-β-treated control fibroblasts and SSc lung fibroblasts. Deletion of the CTGF gene showed reduced bleomycin-induced pulmonary fibrosis in mice. Overall, these results support that CTGF plays a pivotal role in fibrosis and blocking CTGF activity may be useful as a specific target of attenuating fibrosis in SSc.
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Charrier, Alyssa. "Connective Tissue Growth Factor in Pancreatitis." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1366025057.

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Bonniaud, Philippe. "Transforming growth factor-β1, connective tissue growth factor et fibrose pulmonaire." Dijon, 2005. http://www.theses.fr/2005DIJOMU01.

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La fibrose pulmonaire (FP) est une maladie incurable. Nous nous sommes intéressés aux effets pathobiologiques de Transforming growth factor (TGF)βsur la FP. Par adénovecteurs, nous avons transféré à des poumons de rongeurs des cytokines susceptibles d'être impliqués dans la FP-TGF-β1, interleukine (IL)-1β, et connective tissue growth factor (CTGF)-. Nous démontrons que :1) TGFβ est essentiel pour l'initiation et la progression de la FP 2)CTGF est nécessaire mais incapable par lui seul d'induire la progression de la FP. CTGF pourrait être un cofacteur de TGFβ 3)FP et emphysème sont dépendants de Smad3, molécule de signal de TGFβ, démontrant l'importance de TGFβ dans l'équilibre entre accumulation et dégradation de matrice 4)la FP induite par IL-1β est dépendante de TGFβ 5)un inhibiteur spécifique du récepteur ALK5 de TGFβ bloque la FP induite par TGFβ. Conclusion : TGFβet ses voies de signal sont clés dans la FP. Ce travail est une ouverture à des possibilités thérapeutiques.
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Rachfal, Amy Wilson. "Expression and actions of connective tissue growth factor." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1069791086.

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Rachfal, Amy Wilson. "Expression and actions of connective tissue growth factor." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1069791086.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xx, 186 p.; also includes graphics (some col.) Includes bibliographical references (p. 159-186). Available online via OhioLINK's ETD Center
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Wright, Aleksandra. "The roles and interactions of connective tissue growth factor." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434988.

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Huang, Bau-Lin. "Connective tissue growth factor gene regulation and function of CTGF /." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=2026641211&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Yokoi, Hideki. "Role of connective tissue growth factor in renal tubulointerstitial fibrosis." Kyoto University, 2005. http://hdl.handle.net/2433/144757.

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Gebhardt, Susanne. "Expression, biochemische Charakterisierung und biologische Analyse des CONNECTIVE TISSUE GROWTH FACTOR." kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2008/2956/.

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Tang, Xiaodi. "The role of connective tissue growth factor (CTGF) in articular cartilage." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/25292.

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Work from our group has identified an important role for the pericellular matrix (PCM) of cartilage in mechanotransduction. This region of the matrix sequesters regulatory molecules such as fibroblastic growth factor 2 (FGF2) and releases them upon mechanical stimulation. By carrying out a proteomic analysis of PCM proteins we identified an additional regulatory molecule, connective tissue growth factor (CTGF). CTGF was of interest to us as this protein is up-regulated in osteoarthritis but its function in chondrocytes is unknown. I confirmed the pericellular localisation of CTGF in cartilage and showed that it binds to heparan sulphate perlecan and like FGF2, CTGF is rapidly released from the PCM upon cartilage injury. In order to determine its function in chondrocytes, I expressed recombinant CTGF and performed a microarray study in isolated human chondrocytes. Four genes were up- regulated by CTGF and all were known to be transforming growth factor beta (TGFβ) inducible. Recombinant CTGF was able to activate SMAD2 in porcine chondrocytes indicating that it can activate the canonical TGFβ signalling pathway. Both CTGF induced gene expression and SMAD2 phosphorylation was abrogated by TGFβ neutralising antibody and the TGFβ receptor inhibitor SB431542, suggesting that the activity of CTGF is TGFβ dependent. Adding exogenous CTGF to rested porcine cartilage increased TGFβ protein accumulation without affecting TGFβ mRNA levels, suggesting that CTGF may control TGFβ protein’s bioavailability. Injured porcine cartilage caused rapid release of endogenous CTGF as well as a delayed accumulation of TGFβ in the conditioned medium (CM). TGFβ proteins are synthesised and secreted in a latent complex associated with the latency- associated peptide (LAP). When I analysed the explantation CM under non-reducing conditions, CTGF resolved at a high molecular weight (~150kDa), and a high molecular weight fraction of this CM contained SMAD2 activity suggesting that CTGF may be in complex with latent TGFβ. This was supported by the identification of LAP in CTGF immunoprecipitates. Injured cartilage from CTGF knockout mice released reduced levels of CTGF but apparently normal levels of TGFβ suggesting that CTGF is not necessary for release of latent TGFβ. However, SMAD2-phosphorylating ability of the medium was compromised indicating that CTGF controls TGFβ bioavailability principally by facilitating activation of latent complex at the surface of the chondrocyte. These data unveil a novel role for CTGF in cartilage through controlling TGFβ bioavailability.
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Book chapters on the topic "Connective Tissue Growth Factor ECM"

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Salajegheh, Ali. "Connective Tissue Growth Factor (CTGF)." In Angiogenesis in Health, Disease and Malignancy, 47–50. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_9.

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Fujimoto, Manabu, and Kazuhiko Takehara. "Transforming Growth Factor-ß and Connective Tissue Growth Factor." In Systemic Sclerosis, 137–53. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55708-1_9.

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Yin, Qing, and Hong Liu. "Connective Tissue Growth Factor and Renal Fibrosis." In Advances in Experimental Medicine and Biology, 365–80. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2_17.

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Kelley, Jason. "Platelet-Derived Growth Factor, Transforming Growth Factor-β and Connective Tissue Growth Factor." In Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction, 131–53. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7362-8_6.

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Kawanami, Daiji, Saptarsi M. Haldar, and Mukesh K. Jain. "Role of Connective Tissue Growth Factor in Cardiac Fibrosis." In CCN Proteins in Health and Disease, 121–32. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_10.

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Ikegami, Y., and H. Ijima. "Strategies and Advancement in Growth Factor Immobilizable ECM for Tissue Engineering." In Immobilization Strategies, 141–64. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7998-1_3.

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Uzel, Mehmet Ilhan, Hsiang Hsi-Hong, Michael C. Sheff, and Philip C. Trackman. "TGF-ß1 Regulation of Gingival Lysyl Oxidase and Connective Tissue Growth Factor." In Biochemistry and Molecular Biology of Vitamin B6 and PQQ-dependent Proteins, 77–82. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8397-9_13.

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Rowley, David R. "Reactive Stroma and Evolution of Tumors: Integration of Transforming Growth Factor-β, Connective Tissue Growth Factor, and Fibroblast Growth Factor-2 Activities." In Transforming Growth Factor-β in Cancer Therapy, Volume II, 475–505. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-293-9_30.

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Robinson, Paulette M., Timothy D. Blalock, Rong Yuan, Alfred S. Lewin, and Gregory S. Schultz. "Hammerhead Ribozyme-Mediated Knockdown of mRNA for Fibrotic Growth Factors: Transforming Growth Factor-Beta 1 and Connective Tissue Growth Factor." In Methods in Molecular Biology, 117–32. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-439-1_8.

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Wheeler, Jason B., John S. Ikonomidis, and Jeffrey A. Jones. "Connective Tissue Disorders and Cardiovascular Complications: The Indomitable Role of Transforming Growth Factor-β Signaling." In Advances in Experimental Medicine and Biology, 161–84. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80614-9_7.

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Conference papers on the topic "Connective Tissue Growth Factor ECM"

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Alexopoulos, Leonidas G., Mansoor A. Haider, and Farshid Guilak. "An Axisymmetric Elastic Layered Half-Space Model for Micropipette Aspiration of the Chondrocyte Pericellular Matrix." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23156.

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Abstract Articular cartilage is an aneural, avascular connective tissue that serves as the resilient load-bearing surface at the articulating ends of diarthrodial joints. A sparse single population of cells known as chondrocytes maintains the extracellular matrix (ECM) of this tissue through a balance of anabolic and catabolic activities. The mechanical environment of chondrocytes, in conjunction with other genetic and environmental factors (e.g., growth factors, cytokines), plays an important role in regulating cartilage homeostasis and, as a consequence, the health of the joint.
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Kelly, P., E. Nuglozeh, F. Safadi, and S. Popoff. "Creating a Knockout for the Gene Connective Tissue Growth Factor." In Minority Trainee Research Forum, 2004. TheScientificWorld Ltd, 2004. http://dx.doi.org/10.1100/tsw.2004.203.

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Lee, Chang H., Eduardo K. Moioli, and Jeremy J. Mao. "Fibroblastic Differentiation of Human Mesenchymal Stem Cells using Connective Tissue Growth Factor." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.259866.

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Lee, Chang H., Eduardo K. Moioli, and Jeremy J. Mao. "Fibroblastic Differentiation of Human Mesenchymal Stem Cells using Connective Tissue Growth Factor." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4397516.

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Zhong, Jing, Xiaoping Zhu, Hong Zhao, Stephen Tc Wong, and Stephen Tc Wong. "Abstract 4924: Connective tissue growth factor (CTGF) mediates metastases of breast cancer stem cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4924.

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Chaudhary, Priyanka, Marie-Liesse Labat, Guangfang Wang, and Mark Onaitis. "Abstract 3047: Connective tissue growth factor: Novel therapeutic target for non-small cell lung cancer." 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.am2019-3047.

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Chaudhary, Priyanka, Marie-Liesse Labat, Guangfang Wang, and Mark Onaitis. "Abstract 3047: Connective tissue growth factor: Novel therapeutic target for non-small cell lung cancer." 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.sabcs18-3047.

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Kono, Masato, Yutaro Nakamura, Takafumi Suda, Yusuke Kaida, Masato Kato, Dai Hashimoto, Naoki Inui, et al. "N-terminal Connective Tissue Growth Factor (CTGF) Is A Potential Biomarker Of Idiopathic Interstitial Pneumonias (IIPs)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1106.

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Soares, João S., Trung L. Le, Fotis Sotiropoulos, and Michael S. Sacks. "Modeling the Role of Oscillatory Flow and Dynamic Mechanical Conditioning on Dense Connective Tissue Formation in Mesenchymal Stem Cell Derived Heart Valve Tissue Engineering." In ASME 2013 Conference on Frontiers in Medical Devices: Applications of Computer Modeling and Simulation. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/fmd2013-16165.

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Abstract:
Living tissue engineered heart valves (TEHV) may circumvent ongoing problems in pediatric valve replacements, offering optimum hemodynamic performance and the potential for growth, remodeling, and self-repair [1]. Although a myriad of external stimuli are available in current bioreactors (e.g. oscillatory flows, mechanical conditioning, etc.), there remain significant bioengineering challenges in determining and quantifying parameters that lead to optimal ECM development and structure for the long term goal of engineering TEHVs exhibiting tissue architecture functionality equivalent to native tissue. It has become axiomatic that in vitro mechanical conditioning promotes engineered tissue formation (Figure 1), either in organ-level bioreactors or in tissue-level bioreactors with idealized-geometry TE constructs. However, the underlying mechanisms remain largely unknown. Efforts to date have been largely empirical, and a two-pronged approach involving novel theoretical developments and close-looped designed experiments is necessary to reach a better mechanistic understanding of the cause-effect interplay between MSC proliferation and differentiation, newly synthetized ECM, and tissue formation, in response to the controllable conditions such as scaffold design, oxygen tension, nutrient availability, and mechanical environment during incubation. We thus evaluate the influence of exterior flow oscillatory shear stress and dynamic mechanical conditioning on the proliferative and synthetic behavior of MSCs by employing a novel theoretical framework for TE. We employ mixture theory to describe the evolution of the biochemical constituents of the TE construct and their intertwined biochemical reactions, evolving poroelastic models to evaluate the enhancement of nutrient transport occurring with dynamic mechanical deformations, and computational fluid dynamics (CFD) to assess the exterior flow boundary conditions developed in the flex-stretch-flow (FSF) bioreactor [4–6].
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Wang, Ran, Gengyun Sun, and Sijing Zhou. "Cigarette smoking alters microRNA expression profiling and contributes to pulmonary artery remodeling via targeting connective tissue growth factor." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa588.

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