Relevant bibliographies by topics / CCN3

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'CCN3'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "CCN3"

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MacDonald, Iona J., Chien-Chung Huang, Shan-Chi Liu, Yen-You Lin, and Chih-Hsin Tang. "Targeting CCN Proteins in Rheumatoid Arthritis and Osteoarthritis." International Journal of Molecular Sciences 22, no. 9 (April 21, 2021): 4340. http://dx.doi.org/10.3390/ijms22094340.

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The CCN family of matricellular proteins (CYR61/CCN1, CTGF/CCN2, NOV/CCN3 and WISP1-2-3/CCN4-5-6) are essential players in the key pathophysiological processes of angiogenesis, wound healing and inflammation. These proteins are well recognized for their important roles in many cellular processes, including cell proliferation, adhesion, migration and differentiation, as well as the regulation of extracellular matrix differentiation. Substantial evidence implicates four of the proteins (CCN1, CCN2, CCN3 and CCN4) in the inflammatory pathologies of rheumatoid arthritis (RA) and osteoarthritis (OA). A smaller evidence base supports the involvement of CCN5 and CCN6 in the development of these diseases. This review focuses on evidence providing insights into the involvement of the CCN family in RA and OA, as well as the potential of the CCN proteins as therapeutic targets in these diseases.
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Brigstock, DR. "The CCN family: a new stimulus package." Journal of Endocrinology 178, no. 2 (August 1, 2003): 169–75. http://dx.doi.org/10.1677/joe.0.1780169.

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The CCN family comprises cysteine-rich 61 (CYR61/CCN1), connective tIssue growth factor (CTGF/CCN2), nephroblastoma overexpressed (NOV/CCN3), and Wnt-induced secreted proteins-1 (WISP-1/CCN4), -2 (WISP-2/CCN5) and -3 (WISP-3/CCN6). These proteins stimulate mitosis, adhesion, apoptosis, extracellular matrix production, growth arrest and migration of multiple cell types. Many of these activities probably occur through the ability of CCN proteins to bind and activate cell surface integrins. Accumulating evidence supports a role for these factors in endocrine pathways and endocrine-related processes. To illustrate the broad role played by the CCN family in basic and clinical endocrinology, this Article highlights the relationship between CCN proteins and hormone action, skeletal growth, placental angiogenesis, IGF-binding proteins and diabetes-induced fibrosis.
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Wu, Qunfeng, Marda Jorgensen, Joanna Song, Junmei Zhou, Chen Liu, and Liya Pi. "Members of the Cyr61/CTGF/NOV Protein Family: Emerging Players in Hepatic Progenitor Cell Activation and Intrahepatic Cholangiocarcinoma." Gastroenterology Research and Practice 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2313850.

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Hepatic stem/progenitor cells (HPC) reside quiescently in normal biliary trees and are activated in the form of ductular reactions during severe liver damage when the replicative ability of hepatocytes is inhibited. HPC niches are full of profibrotic stimuli favoring scarring and hepatocarcinogenesis. The Cyr61/CTGF/NOV (CCN) protein family consists of six members, CCN1/CYR61, CCN2/CTGF, CCN3/NOV, CCN4/WISP1, CCN5/WISP2, and CCN6/WISP3, which function as extracellular signaling modulators to mediate cell-matrix interaction during angiogenesis, wound healing, fibrosis, and tumorigenesis. This study investigated expression patterns of CCN proteins in HPC and cholangiocarcinoma (CCA). Mouse HPC were induced by the biliary toxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). Differential expression patterns of CCN proteins were found in HPC from DDC damaged mice and in human CCA tumors. In addition, we utilized reporter mice that carried Ccn2/Ctgf promoter driven GFP and detected strong Ccn2/Ctgf expression in epithelial cell adhesion molecule (EpCAM)+ HPC under normal conditions and in DDC-induced liver damage. Abundant CCN2/CTGF protein was also found in cytokeratin 19 (CK19)+ human HPC that were surrounded by α-smooth muscle actin (α-SMA)+ myofibroblast cells in intrahepatic CCA tumors. These results suggest that CCN proteins, particularly CCN2/CTGF, function in HPC activation and CCA development.
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Mo, Fan-E., Andrew G. Muntean, Chih-Chiun Chen, Donna B. Stolz, Simon C. Watkins, and Lester F. Lau. "CYR61 (CCN1) Is Essential for Placental Development and Vascular Integrity." Molecular and Cellular Biology 22, no. 24 (December 15, 2002): 8709–20. http://dx.doi.org/10.1128/mcb.22.24.8709-8720.2002.

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ABSTRACT CYR61 (CCN1) is a member of the CCN family of secreted matricellular proteins that includes connective tissue growth factor (CCN2), NOV (CCN3), WISP-1 (CCN4), WISP-2 (CCN5), and WISP-3 (CCN6). First identified as the product of a growth factor-inducible immediate-early gene, CYR61 is an extracellular matrix-associated angiogenic inducer that functions as a ligand of integrin receptors to promote cell adhesion, migration, and proliferation. Aberrant expression of Cyr61 is associated with breast cancer, wound healing, and vascular diseases such as atherosclerosis and restenosis. To understand the functions of CYR61 during development, we have disrupted the Cyr61 gene in mice. We show here that Cyr61-null mice suffer embryonic death: ∼30% succumbed to a failure in chorioallantoic fusion, and the reminder perished due to placental vascular insufficiency and compromised vessel integrity. These findings establish CYR61 as a novel and essential regulator of vascular development. CYR61 deficiency results in a specific defect in vessel bifurcation (nonsprouting angiogenesis) at the chorioallantoic junction, leading to an undervascularization of the placenta without affecting differentiation of the labyrinthine syncytiotrophoblasts. This unique phenotype is correlated with impaired Vegf-C expression in the allantoic mesoderm, suggesting that CYR61-regulated expression of Vegf-C plays a role in vessel bifurcation. The genetic and molecular basis of vessel bifurcation is presently unknown, and these findings provide new insight into this aspect of angiogenesis.
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Peng, Linan, Yingying Wei, Yijia Shao, Yi Li, Na Liu, and Lihua Duan. "The Emerging Roles of CCN3 Protein in Immune-Related Diseases." Mediators of Inflammation 2021 (May 18, 2021): 1–8. http://dx.doi.org/10.1155/2021/5576059.

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The CCN proteins are a family of extracellular matrix- (ECM-) associated proteins which currently consist of six secreted proteins (CCN1-6). CCN3 protein, also known as nephroblastoma overexpressed protein (NOV), is a member of the CCN family with multiple biological functions, implicated in major cellular processes such as cell growth, migration, and differentiation. Recently, CCN3 has emerged as a critical regulator in a variety of diseases, including immune-related diseases, including rheumatology arthritis, osteoarthritis, and systemic sclerosis. In this review, we will briefly introduce the structure and function of the CCN3 protein and summarize the roles of CCN3 in immune-related diseases, which is essential to understand the functions of the CCN3 in immune-related diseases.
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Resovi, Andrea, Patrizia Borsotti, Tommaso Ceruti, Alice Passoni, Massimo Zucchetti, Alexander Berndt, Bruce L. Riser, Giulia Taraboletti, and Dorina Belotti. "CCN-Based Therapeutic Peptides Modify Pancreatic Ductal Adenocarcinoma Microenvironment and Decrease Tumor Growth in Combination with Chemotherapy." Cells 9, no. 4 (April 13, 2020): 952. http://dx.doi.org/10.3390/cells9040952.

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The prominent desmoplastic stroma of pancreatic ductal adenocarcinoma (PDAC) is a determinant factor in tumor progression and a major barrier to the access of chemotherapy. The PDAC microenvironment therefore appears to be a promising therapeutic target. CCN2/CTGF is a profibrotic matricellular protein, highly present in the PDAC microenvironment and associated with disease progression. Here we have investigated the therapeutic value of the CCN2-targeting BLR100 and BLR200, two modified synthetic peptides derived from active regions of CCN3, an endogenous inhibitor of CCN2. In a murine orthotopic PDAC model, the two peptides, administered as monotherapy at low doses (approximating physiological levels of CCN3), had tumor inhibitory activity that increased with the dose. The peptides affected the tumor microenvironment, inhibiting fibrosis and vessel formation and reducing necrosis. Both peptides were active in preventing ascites formation. An increased activity was obtained in combination regimens, administering BLR100 or BLR200 with the chemotherapeutic drug gemcitabine. Pharmacokinetic analysis indicated that the improved activity of the combination was not mainly determined by the substantial increase in gemcitabine delivery to tumors, suggesting other effects on the tumor microenvironment. The beneficial remodeling of the tumor stroma supports the potential value of these CCN3-derived peptides for targeting pathways regulated by CCN2 in PDAC.
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Perbal, B. "CCN3-mutant mice are distinct from CCN3-null mice." Journal of Cell Communication and Signaling 1, no. 3-4 (December 2007): 229–30. http://dx.doi.org/10.1007/s12079-008-0020-8.

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McCallum, Lynn M. R., Wanhua Lu, Susan Price, Nathalie Planque, Bernard Perbal, Andrew Pierce, Anthony Whetton, and Alexandra E. Irvine. "BCR-ABL Decreases the Expression of CCN3 Leading to Increased Clonogenic Potential and Cell Growth." Blood 106, no. 11 (November 16, 2005): 1216. http://dx.doi.org/10.1182/blood.v106.11.1216.1216.

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Abstract Chronic Myeloid Leukemia (CML) is characterized by expression of the constitutively active BCR-ABL tyrosine kinase. Previously, we have identified downregulation of the negative growth regulator, CCN3, as a result of BCR-ABL kinase activity and detected reduced CCN3 expression in human CML cell lines and primary human CML cells. We now report a reciprocal relationship of BCR-ABL and CCN3 expression and the functional consequence of expressing CCN3 in BCR-ABL+ cells. Real-time PCR was used to examine the relationship between BCR-ABL and CCN3 expression in human K562 cells. Parental K562 cells showed high expression of BCR-ABL (4.68 x104 transcripts in 5 μL of cDNA) whilst CCN3 expression was not detected. Treatment with siRNA directed against BCR-ABL (0.5 μg per106 cells) for 72 hours resulted in a 3.7 fold decrease in BCR-ABL and 6.1 fold increase in CCN3 expression (mean Ct change 1.9 ± 0.2 and 2.6 ± 0.5 for BCR-ABL and CCN3 respectively, n=3, p=0.001). Similarly, K562 cells treated with imatinib (1 micromolar) for 96 hours showed a 5.9 fold decrease in BCR-ABL expression and a 4.2 fold increase in CCN3 expression (mean Ct change 2.5 ± 0.1 and 2.1± 0.2 for BCR-ABL and CCN3 respectively, n=3, p=0.001). To investigate CCN3 function, we expressed CCN3 in BCR-ABL+ cells using Nucleofector technology (Amaxa, GmbH). K562 cells were transfected with either the pCb6+ vector (Invitrogen,UK) or pCb6+ vector containing the CCN3 construct. Cells were analysed 24 hours post-transfection by flow cytometry and also after 7 days in methyl cellulose culture to determine clonogenicity. Cell cycle analysis was performed on 20,000 events using the winMDI software. CCN3 expression in BCR-ABL+ cells resulted in an accumulation of cells in the subG0 phase of the cell cycle (mean for subG0 9.9% ± 4.6 and 21.8% ± 0.7 for the pCb6+ vector alone and pCb6+ vector containing CCN3 construct respectively). CCN3 expression significantly increased the number of cells within the subG0 area of the cell cycle (n=3, p=0.027). In addition, CCN3 expression reduced the clonogenic capacity of BCR-ABL+ cells. K562 cells transfected with the pCb6+ vector containing CCN3 construct formed significantly fewer colonies on methyl cellulose in comparison to cells that had been transfected with the pCb6+ vector alone (n=3, p=0.027). This study demonstrates a reciprocal relationship between CCN3 and BCR-ABL expression. CCN3 is known to be a negative growth regulator and increased expression of CCN3 in BCR-ABL+ cells inhibits proliferation and decreases clonogenic potential. Thus CCN3 down-regulation mediated by BCR-ABL offers growth advantage to hematopoietic cells.
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Ouellet, VéRonique, Matthew Dankner, Laudine Desreumaux-Communal, Estelle Schmitt, Dru Perkins, Matthew G. Annis, Veronique Barres, et al. "CCN3/NOV as a functional driver and prognostic biomarker of prostate cancer bone metastasis." Journal of Clinical Oncology 37, no. 7_suppl (March 1, 2019): 182. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.182.

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182 Background: Prostate cancer commonly metastasizes to the bone, resulting in pathological fractures and poor prognosis. CCN3/NOV (Nephroblastoma overexpressed) has been implicated in promoting the formation of osteolytic prostate cancer (PC) bone metastases. The C-terminal domain of CCN3 binds growth factors, heparin sulfate proteoglycans, activates Notch signaling and promotes dimerization of CCN family members. We hypothesize that the CCN3 CT domain is required to promote osteolytic PC bone metastasis and that CCN3 represents a prognostic biomarker in primary PC tumors to predict recurrence to bone. Methods: CCN3WT and CCN3∆CT were overexpressed in LNCaP C4-2 cells. The role of CCN3 was assessed with in vitro proliferation, migration and invasion assays, and in vivo through intracardiac injection in male Nude mice (Nu/Nu). Ex vivo µCT scans were performed on bone specimens. CCN3 expression was assessed in two unique tissue microarrays (TMA) comprising over 1,500 primary prostate tumor using different anti-CCN3 antibodies with immunohistochemistry and immunohistofluorescnece, respectively. Results: While CCN3WT and CCN3∆CT had little effect in vitro on cell proliferation, migration or invasion, intracardiac injection of CCN3WT resulted in increased incidence of bone metastasis compared to empty vector control and CCN3∆CT. Ex vivo µCT revealed decreased bone mineral density in bones from mice injected with CCN3WT cells compared to control and CCN3∆CT expressing cells. In both TMAs studied, high CCN3 expression in tumor epithelium correlated with increased risk of biochemical relapse and bone metastasis at 5 years and 15 years post-resection, respectively. Conclusions: CCN3 requires its C-terminal domain for its bone metastatic function, and CCN3 is correlated with aggressive disease biology in prostate cancer. These findings point to CCN3 as a biomarker that can be useful to predict prostate cancer aggressiveness, while providing clarity on its role as a functional mediator of prostate cancer bone metastasis.
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Riser, Bruce L., Feridoon Najmabadi, Bernard Perbal, Jo Ann Rambow, Melisa L. Riser, Ernest Sukowski, Herman Yeger, Sarah C. Riser, and Darryl R. Peterson. "CCN3/CCN2 regulation and the fibrosis of diabetic renal disease." Journal of Cell Communication and Signaling 4, no. 1 (February 9, 2010): 39–50. http://dx.doi.org/10.1007/s12079-010-0085-z.

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Dissertations / Theses on the topic "CCN3"

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Kipkeew, Friederike [Verfasser], Elke [Akademischer Betreuer] Winterhager, and Andrea [Akademischer Betreuer] Vortkamp. "Die CCN Proteine CCN1 (CYR61) und CCN3 (NOV) : Regulatoren der Trophoblastproliferation und -migration / Friederike Kipkeew. Gutachter: Andrea Vortkamp. Betreuer: Elke Winterhager." Duisburg, 2014. http://d-nb.info/1049647432/34.

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Bohr, Wilhelm [Verfasser]. "Expression, Aufreinigung und Charakterisierung von rekombinantem hCTGF (CCN2) und rNOV (CCN3) in einem eukaryontischen Zellsystem / Wilhelm Bohr." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2010. http://d-nb.info/1015149219/34.

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Guo, Yanping. "The mechanism of Nov (CCN3) function in haematopoiesis." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:5785f3b9-3206-4bb4-b486-d90cded680f8.

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Haematopoietic stem cells (HSC) are strictly regulated by intrinsic regulators and extrinsic signals from the microenvironment. Nov (CCN3), a matricellular protein of the CCN family, has been reported as a suppressor gene in solid tumours and chronic myeloid leukaemia (CML). Recent study identified Nov as a positive regulator in human cord blood CD34+ stem cells. However, the functions of Nov in haematopoiesis and adult HSC remain largely unknown.
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Le, Dréau Gwenvaël. "NOV/CCN3 et système nerveux central : étude du rôle de NOV/CCN3 dans les précurseurs de neurones granulaires et des astrocytes." Paris 6, 2008. http://www.theses.fr/2008PA066063.

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NOV/CCN3 est une protéine sécrétée et multifonctionnelle impliquée dans le développement de différents tissus. Le système nerveux central représentant l’un de ses sites majeurs d’expression au cours du développement, nous avons ainsi émis l’hypothèse que NOV participe au développement de ce tissu. Les résultats obtenus en étudiant le rôle potentiel de NOV durant la phase postnatale de développement du cervelet chez le rat suggèrent que NOV participe à la mise en place des neurones granulaires en inhibant la prolifération et stimulant la migration de leurs précurseurs. Par ailleurs, nous avons observé in vitro que l’expression de NOV est induite au cours de la différenciation de lignées de précurseurs astrocytaires mais que NOV ne semble pas réguler ce processus. Ces résultats soutiennent l’hypothèse que NOV soit impliquée dans le développement du système nerveux central, en particulier dans le devenir de populations neuronales.
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Lu, W. "Characterisation of CCN3 signalling pathway in Chronic Myeloid Leukaemia (CML)." Thesis, Queen's University Belfast, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517404.

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Li, Chang Long. "Etude de la protéine CCN3/NOVH dans la signalisation cellulaire." Paris 7, 2003. http://www.theses.fr/2003PA077223.

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Ricard, Anne-Sophie. "Les molécules d’adhésion CCN3 et DDR1 au cours du vitiligo." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21854/document.

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Le vitiligo généralisé est une leucodermie acquise qui touche 0,5 à 1% de la population mondiale et qui résulte d’une perte progressive des mélanocytes.Le mécanisme à l’origine de la perte des mélanocytes au cours du vitiligo reste obscur et la destruction des mélanocytes n’a jamais été observée.De nombreuses hypothèses ont été avancées pour expliquer la disparition des mélanocytes : une susceptibilité génétique, l’auto-immunité, la théorie neurale et la théorie oxydative.Notre équipe a développé une théorie intégrée qui reprend ces différents mécanismes. Cette théorie considère que le vitiligo est lié au détachement des mélanocytes et à leur élimination à travers l’épiderme ou mélanocytorrhagie. Dans cette théorie, un défaut d’adhésion des mélanocytes est le facteur prédisposant au vitiligo.L’interaction des mélanocytes avec les kératinocytes environnants et avec la membrane basale est médiée par les intégrines et les cadhérines. L’expression de l’intégrine et de la E-cadhérine n’est pas modifiée dans le vitiligo généralisé.En 2006, Fukunaga-Kalabis et al. montrent que l’attachement des mélanocytes à la membrane basale est en partie dû à DDR1 qui est sous le contrôle de la protéine CCN3. Ils ont observé que l’inhibition de CCN3 induit le détachement des mélanocytes.Récemment, des variants génétiques de DDR1 ont été observés chez des patients d’origine ethnique différente atteints de vitiligo. Nous avons décidé d’étudier d’une part l’expression de CCN3 au niveau de la peau lésionnelle et non lésionnelle de patients atteints de vitiligo et d’autre part l’impact de l’inhibition de CCN3 et de DDR1 au niveau de mélanocytes utilisés pour des reconstructions épidermiques. Nos résultats in vitro et in vivo suggèrent que CCN3 est impliqué dans la physiopathologie du vitiligo
Common generalized vitiligo is an acquired hypopigmentation which is found in 0, 5-1% of individuals world-wide and which results in progressive loss of melanocytes.The mechanism underlying the elimination of melanocytes in vitiligo remains unclear and melanocyte destruction has never been clearly demonstrated in non segmental vitiligo. Various hypotheses have been put forward to explain the disappearance of melanocytes in vitiligo: genetic susceptibility, autoimmunity, neural and impared redox status. We previously proposed a new theory that integrates those pathomechanisms. This theory considers vitiligo as a disease caused by the chronic detachment and transepidermal loss of melanocytes named melanocytorrhagy. In this theory, the defective adhesion of melanocytes is the predisposing factor.Interactions between melanocytes and the basement membrane are mediated by integrins and interactions between melanocytes and keratinocytes are mediated by cadherins in association with β-catenin. But integrin expression is not affected in NSV and a normal expression of E-cadherin in lesional and non lesional vitiligo skin is observed.In 2006, Fukunaga-Kalabis et al. reported that attachment of melanocytes to basal lamina is in part due to DDR1, which is under control of CCN3. They have observed that inhibition of CCN3 induces the detachment of melanocytes.Recently, DDR1 genetics variants have been associated with vitiligo in patients of different ethnic origin. We have decided to study in parallel the expression of CCN3 and DDR1 in lesional and non lesional skin of vitiligo patients and the impact of inhibition of CCN3 and DDR1 in melanocytes on their behaviour in reconstructed epidermis.In conclusion, our in vivo and in vitro data suggest that CCN3 is implicated in vitiligo etiology
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Wang, Wen. "Investigating the role of CCN1, CCN2, and CCN6 in osteoclast and osteoblast physiology." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=204059.

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CCN protein family members (CYR61, CTGF, Nov, Wisp-1, Wisp-2 and Wisp-3) have important roles in many different processes including angiogenesis, inflammation, remodelling of extracellular matrix and tumorigenesis. In bone, CCN1 increases osteoblastogenesis via Wnt3A signalling and activation of -catenin which, in turn, upregulates CCN1 expression. The exact role of CCN1, CCN2, and CCN6 in osteoclast physiology are not known but we have recently shown that recombinant human (rh)CCN1 inhibits osteoclastogenesis in vitro. The aim of this study was to determine: 1) the expressions of all six members of the CCN protein family in osteoblasts and osteoclasts; 2) the functions of recombinant human CCN2, CCN6 in osteoclastogenesis; 3) whether osteoblast-derived CCN1 may mediate the effect of CCN1 on osteoclast formation and the roles of osteoblast-derived CCN1 and/or osteoclast-derived CCN1 in osteoblast and/or osteoclast differentiation; 4) which signalling pathways are involved in the function of CCN1 in osteoclasts and osteoblasts. We found CCN1-5 but not CCN6 expressed in murine osteoclasts and osteoblasts. All six members were expressed in human OA osteoblasts but only CCN1-3 were detected in human osteoclasts using quantitative RT-PCR. rhCCN1 (in agreement with our previous observations), and also 2 and 6 inhibited human and mouse osteoclast formation in a concentration-dependent manner. We generated and validated an expression construct to specifically overexpress CCN1 in osteoblasts. Incorporation of CCN1-specific siRNA reduced CCN1 expression to between 12.5% and 50% of control osteoblast cultures. In both co-cultures with direct contact between osteoblasts and osteoclast co-cultures as well as Transwell cultures, overexpression of CCN1 in osteoblasts decreased the formation of TRAP positive multinucleated osteoclast-like cells, while siRNA mediated knockdown of CCN1 in the osteoblasts resulted in increased osteoclast-like cell formation. These data suggest that osteoblast-derived CCN1 is a secreted negative regulator of osteoclastogenesis. Moreover, overexpression or knockdown of CCN1 in osteoclast precursors inhibited or increased osteoclast differentiation whilst overexpression or knockdown CCN1 in osteoblasts increased or inhibited osteoblast mineralization respectively. Further investigation found that CCN1 increased Wnt and MAPK signalling in osteoblasts cultured in mineralization medium and inhibited Wnt and IGF-1 signalling during osteoclast differentiation. In conclusion, paracrine and autocrine effects of CCN1 have been demonstrated in osteoclasts and osteoblasts in this study and Wnt, MAPK, amd IGF-1 signalling pathways, may be involved in these effects.
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O''''Hagan, Thomas P. "The role of regulatory T cells and CCN3 in CNS myelination and remyelination." Thesis, Queen's University Belfast, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.728386.

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Multiple Sclerosis (MS) is an immune-mediated disease, characterised by demyelination in the central nervous system (CNS)- In MS, the regeneration of myelin sheaths (remyelination) can occur. However, when this regenerative process fails, patients can develop permanent disability. The promotion of remyelination is currently an unmet clinical need that holds significant potential to improve the lives of MS patients. Despite the pathological role of CD4+ T cells in MS, T cells have been shown to support remyelination in experimental models. However, previous studies have investigated total CD4+ T cells without addressing distinct CD4+ T cell subsets. CD4+ Regulatory T cells (Treg) have been identified in multiple organ systems as having a role in repair and regeneration; therefore, we aimed to characterise the role of the anti-inflammatory, CD4+ T cell subset, Treg, in CNS remyelination. To determine if Treg have a direct effect on neural cells we utilised an organotypic brain stem slice model that myelinates ex vivo. In both inflammatory and stabilised brain slice cultures, Treg and/or conditioned media from Treg cultures promoted the maturation of oligodendrocytes, developmental myelination and remyelination as measured by the co-localisation of fluorescent staining of myelin and axons. Treg-deficient mice exhibited impaired oligodendrocyte differentiation during remyelination that was rescued by the adoptive transfer of Treg in vivo. Proteome profiling of conditioned media identified CCN3 as a novel Treg-derived factor that promoted myelination and was required for Treg-enhanced myelination in brain slices. This is the first evidence of CCN3 in CNS regeneration and of CCN3 production by T cells. These findings uncover a new role of Treg in promoting oligodendrocyte differentiation and remyelination in the CNS, distinct from, but complementary to, the classical anti-inflammatory roles of Treg.
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Marchal, Pierre-Olivier. "Rôle de NOV/CCN3 dans différents modèles in vivo de néphropathies et pathologies cardiovasculaires." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066321.

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La maladie rénale chronique (MRC) est un véritable problème de santé publique. Bien qu'elle puisse avoir plusieurs origines, celle-ci est caractérisée par le développement d'une inflammation chronique ainsi qu'une fibrose conduisant à une diminution progressive de la fonction rénale. Il est nécessaire de trouver de nouvelles cibles thérapeutiques pour arrêter la progression de cette pathologie. La protéine NOV/CCN3 a été identifiée comme étant une cible potentiellement intéressante. Dans cette étude, nous avons montré que dans un modèle in vivo de néphropathie obstructive, NOV avait un rôle proinflammatoire et profibrotique. Dans un autre modèle in vivo de néphropathie hypertensive, nous avons montré que NOV était régulée par l'Angiotensine II (AngII) et pouvait inhiber l'expression du récepteur AT1R de l'AngII et ainsi limiter les effets délétères de cette hormone. Bien que contradictoires, ces résultats montrent un rôle important de NOV au cours du développement des néphropathies indiquant que cette protéine peut avoir des effets opposés en fonction du contexte pathologique. Enfin, du fait de l'étroite relation entre NOV et l'AngII, nous avons montré que NOV était aussi régulée par cette hormone au niveau aortique et avait un effet proinflammatoire au niveau vasculaire dans des conditions d'hypertension. L'ensemble de nos résultats montrent un rôle important de NOV dans ces différents types de pathologies et que cette protéine pourrait être une cible intéressante pour traiter les néphropathies ou encore les pathologies cardiovasculaires
Chronic kidney disease (CKD) is a major public health problem. Regardless of the primary cause, CKD is characterized by the development of chronic inflammation and fibrosis leading to progressive decline of renal function and eventually end-stage renal disease (ESRD). Actually, regular hemodialysis and renal transplantation are the only available therapies for ESRD patients. Therefore, there is an urgent need for new therapeutically targets against this incurable disease. Recently, the NOV/CNN3 protein was shown to be an interesting candidate. In this study we have shown that, in obstructive nephropathy in mice, NOV has profinflammatory and profibrotic effects. In addition, we have shown in a mouse model of hypertensive nephropathy, that NOV was regulated by Angiotensin II (AngII) and could inhibit AT1R receptor expression to limit the deleterious effects of this hormone. These results show an important role of NOV during the development of two different types of nephropathies and may indicate that this protein can have model specific effects. Finally, we have shown that NOV itself was also regulated by AngII in the aorta and has proinflammatory effects in hypertensive conditions. Taken together our results show an important role of NOV in these different types of pathologies and that this protein could be a key player in the development of CKD as well as vascular diseases. Nevertheless, further investigations are still required to better characterize the precise role of NOV in these pathological contexts
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Books on the topic "CCN3"

1

Minutella, David. CCNA. [Indianapolis, Ind.]: Que Certification, 2006.

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Minutella, David. CCNA. [Indianapolis, Ind.]: Que Certification, 2006.

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Jeremy, Cioara, and Stevenson Heather, eds. CCNA. [Indianapolis, Ind.]: Que Certification, 2006.

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Lammle, Todd. CCNA. New York: John Wiley & Sons, Ltd., 2007.

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Minutella, David. CCNA. [Indianapolis, Ind.]: Que Certification, 2006.

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Sheldon, Barry, ed. CCNA. Indianapolis, Ind: Que, 2004.

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Valentine, Michael. CCNA. 3rd ed. [Indianapolis, Ind.]: Que Pub., 2008.

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Odom, Sean. CCNP support. Scottsdale, AZ: Coriolis Group Books, 2001.

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Ciccarelli, Patrick. CCNA jumpstart. San Francisco: Sybex, 1999.

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Inc, Cisco Systems, ed. CCNP practical studies : troubleshooting : CCNP self-study. Indianapolis, Ind: Cisco, 2003.

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Book chapters on the topic "CCN3"

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Hattori, Takako, Mitsuhiro Hoshijima, and Masaharu Takigawa. "Protein Imaging of CCN2 and CCN3 in Living Cells." In Methods in Molecular Biology, 211–15. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6430-7_20.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CCN3: NOV, IGFBP9, IGFBP-rP3." In Encyclopedia of Signaling Molecules, 282. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100183.

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Perbal, B. "The CCN3 Protein and Cancer." In New trends in cancer for the 21st century, 23–40. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/978-1-4020-5133-3_3.

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Perbal, Bernard. "A Recent Breakthrough in the CCN Field: Functional Interactions Between CCN2 and CCN3 are Uncovered." In CCN Proteins in Health and Disease, 1–4. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_1.

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Takigawa, Masaharu, Harumi Kawaki, Satoshi Kubota, Karen M. Lyons, and Bernard Perbal. "Cooperative Regulation of Cell Proliferation and Differentiation by CCN2 and CCN3." In CCN Proteins in Health and Disease, 105–9. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_8.

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McCallum, Lynn, and Alexandra E. Irvine. "CCN3: A NOVel Growth Factor in Leukaemia." In CCN Proteins in Health and Disease, 213–21. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_16.

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Perbal, Bernard, Noureddine Lazar, Diana Zambelli, Monia Zuntini, Massimo Serra, Jose Antonio Lopez-Guerrero, Antonio Llombart-Bosch, Piero Picci, and Katia Scotlandi. "Prognostic Relevance of CCN3 in Bone Sarcomas." In CCN Proteins in Health and Disease, 223–43. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_17.

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Katsube, Ken-Ichi. "The Role of CCN3 in Mesenchymal Stem Cells." In CCN Proteins in Health and Disease, 111–19. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_9.

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Riser, Bruce L., Feridoon Najmabadi, Bernard Perbal, Jo Ann Rambow, Melisa L. Riser, Ernest Sukowski, Herman Yeger, Sarah C. Riser, and Darryl R. Peterson. "CCN3 (NOV): A Negative Regulator of CCN2 (CTGF) Activity and an Endogenous Inhibitor of Fibrosis in Experimental Diabetic Nephropathy." In CCN Proteins in Health and Disease, 163–81. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_13.

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Vallacchi, Viviana, Maria Daniotti, Annamaria De Filippo, Licia Rivoltini, Bernard Perbal, and Monica Rodolfo. "CCN3 Promotes Melanoma Progression by Regulating Integrin Expression, Adhesion and Apoptosis Induced by Cytotoxic Drugs." In CCN Proteins in Health and Disease, 205–11. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3779-4_15.

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Conference papers on the topic "CCN3"

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Dankner, Matthew, Veronique Ouellet, Laudine Desreumaux-Communal, Estelle Schmitt, Dru Perkins, Matthew G. Annis, Veronique Barres, et al. "Abstract 3134: CCN3 is a prognostic biomarker and functional mediator of prostate cancer bone metastasis." 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.am2019-3134.

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Chen, Ruei-Ching. "Abstract 5293: CCN3 increases motility of human chondrosarcoma via PI3K, AKT and NF-κB pathways." 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.am10-5293.

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Dankner, Matthew, Veronique Ouellet, Laudine Desreumaux-Communal, Estelle Schmitt, Dru Perkins, Matthew G. Annis, Veronique Barres, et al. "Abstract 3134: CCN3 is a prognostic biomarker and functional mediator of prostate cancer bone metastasis." 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.sabcs18-3134.

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Amir, E., V. Ouellet, A. Mourskaia, K. Tiedemann, J. Fong, D. Tran-Tanh, M. Clemons, B. Perbal, S. Komorova, and PM Siegel. "Abstract P6-07-01: CCN3 Impairs Osteoblasts and Stimulates Osteoclast Differentiation To Favor Breast Cancer Metastasis to Bone." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p6-07-01.

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Chen, Po-Chun, Chia-Chia Chao, An-Chen Chang, and Chih-Hsin Tang. "Abstract LB-099: Prostate cancer-secreted CCN3/NOV promotes osteoblast differentiation via Wnt signal pathway and miR-608 suppression." 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-lb-099.

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Chen, Po-Chun, Chih-Hsin Tang, and Hsu-Chen Cheng. "Abstract 1399: CCN3 enhances migration and ICAM-1 upregulation via avb3 integrin, ILK, Akt, and NF-kB-dependent pathway in human prostate cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1399.

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Cabral, Carlos M. S., Christian Esteve Rothenberg, and Maurício Ferreira Magalhães. "Mini-CCNx." In the 3rd ACM SIGCOMM workshop. New York, New York, USA: ACM Press, 2013. http://dx.doi.org/10.1145/2491224.2491236.

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"CCNC Patrons." In 2008 5th IEEE Consumer Communications and Networking Conference. IEEE, 2008. http://dx.doi.org/10.1109/ccnc08.2007.5.

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Chen, Qingtian, Muhammad Khan, Christina Tsangouri, Christopher Yang, Bing Li, Jizhong Xiao, and Zhigang Zhu. "CCNY Smart Cane." In 2017 IEEE 7th Annual International Conference on CYBER Technology in Automation, Control, and Intelligent Systems (CYBER). IEEE, 2017. http://dx.doi.org/10.1109/cyber.2017.8446303.

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"CCNC 2019 Committees." In 2019 16th IEEE Annual Consumer Communications & Networking Conference (CCNC). IEEE, 2019. http://dx.doi.org/10.1109/ccnc.2019.8651685.

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Reports on the topic "CCN3"

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Mosko, M., I. Solis, and C. Wood. Content-Centric Networking (CCNx) Semantics. RFC Editor, July 2019. http://dx.doi.org/10.17487/rfc8569.

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Hudson, James G. CCN Spectral Measurements. Office of Scientific and Technical Information (OSTI), February 2009. http://dx.doi.org/10.2172/948468.

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Mosko, M., I. Solis, and C. Wood. Content-Centric Networking (CCNx) Messages in TLV Format. RFC Editor, July 2019. http://dx.doi.org/10.17487/rfc8609.

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Hudson, J. G. An instantaneous CCN (cloud condensation nucleus) spectrometer. Office of Scientific and Technical Information (OSTI), May 1989. http://dx.doi.org/10.2172/6159445.

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Boyle, J. S. Comparison of CCM3 simulations using two climatological ozone data sets. Office of Scientific and Technical Information (OSTI), February 1997. http://dx.doi.org/10.2172/632787.

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Uin, Janek. Cloud Condensation Nuclei Particle Counter (CCN) Instrument Handbook. Office of Scientific and Technical Information (OSTI), April 2016. http://dx.doi.org/10.2172/1251411.

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Hudson, James G. CCN Spectra Measurements as an Active Tracer of Stratocumulus Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, October 1992. http://dx.doi.org/10.21236/ada255678.

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Wissingh, B., C. Wood, A. Afanasyev, L. Zhang, D. Oran, and C. Tschudin. Information-Centric Networking (ICN): Content-Centric Networking (CCNx) and Named Data Networking (NDN) Terminology. RFC Editor, June 2020. http://dx.doi.org/10.17487/rfc8793.

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Ziemann, Paul J., Sonia M. Kreidenweis, and Markus D. Petters. Quantifying the Relationship between Organic Aerosol Composition and Hygroscopicity/CCN Activity. Office of Scientific and Technical Information (OSTI), June 2013. http://dx.doi.org/10.2172/1086826.

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Oran, D. Considerations in the Development of a QoS Architecture for CCNx-Like Information-Centric Networking Protocols. RFC Editor, June 2021. http://dx.doi.org/10.17487/rfc9064.

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