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Relevant bibliographies by topics / Collagen Type 1 CTGF

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Academic literature on the topic 'Collagen Type 1 CTGF'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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Journal articles on the topic "Collagen Type 1 CTGF"

1

Takeuchi, H., S. Kubota, E. Murakashi, Y. Zhou, K. Endo, P. S. Ng, M. Takigawa, and Y. Numabe. "Nicotine-induced CCN2: from Smoking to Periodontal Fibrosis." Journal of Dental Research 89, no. 1 (December 4, 2009): 34–39. http://dx.doi.org/10.1177/0022034509353403.

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Since fibrosis is observed in smokers’ gingiva, it was hypothesized that fibrosis was caused by nicotine in the periodontium. Therefore, in this study, we investigated the effects of nicotine on the induction of a profibrotic molecule, connective tissue growth factor (CCN2/CTGF), in human gingival fibroblasts (HGFs) and periodontal ligament (PDL) cells. With 1 μg/mL nicotine, vacuolization and attenuated proliferation were observed. Interestingly, 1 μg/mL nicotine increased the production of CCN2/CTGF protein in both cells without increasing mRNA expression. Furthermore, type I collagen mRNA and protein were also increased and were significantly blocked by a CCN2/CTGF neutralizing antibody. This is the first report to describe a relationship between nicotine and CCN2/CTGF in periodontal tissue cells. Analysis of our data also indicated that nicotine was cytotoxic, while it increased CCN2/CTGF and, eventually, type I collagen production. These findings suggest that periodontal fibrosis can be promoted by nicotine from smoking via effects on CCN2/CTGF.

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Romero, Jose R., Dennis A. Ricupero, Alicia Rivera, Ronald H. Goldstein, and Paul R. Conlin. "Activation of Na + /Ca 2+ Exchanger in Kinin B 1 Receptor-Stimulated Human Fibroblast Is Associated with Collagen Production." Hypertension 36, suppl_1 (October 2000): 710–20. http://dx.doi.org/10.1161/hyp.36.suppl_1.710.

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P148 The arterial wall in hypertension is characterized by thickening of the media, in part due to increased deposition of connective tissue. Autocrine and paracrine factors may participate in this process; including products of the kallikrein-kinin system. We evaluated early signal transduction events and effects on collagen formation in B 1 -stimulated human myofibroblast cells (IMR-90). We measured cytosolic calcium (Ca cyt ) levels in cells loaded with FURA-2AM. Gene expression of connective tissue growth factor (CTGF) and α1(I) collagen was determined by estimating mRNA levels using Northern analysis of B 1 stimulated cells. Activation of the B 1 receptor with des-arg 10 -kallidin stimulated a three-fold increase in CTGF mRNA by increasing its stability. Furthermore, B 1 receptor activation caused an increase in α1(I) collagen mRNA and a four-fold increase in type I collagen synthesis in these cells; events not observed in B 2 receptor-stimulated cells. Activation of the B 1 receptor stimulated a dose dependent rise in Ca cyt (EC 50 =1.9nM) which was completely inhibited by des-arg 10 -[leu 9 ]-kallidin (100nM), a B 1 receptor antagonist. Isosmotic replacement of extracellular Na + with N -methyl,D-glucamine blocked > 90% of the B 1 stimulated rise in Ca cyt . A similar effect was observed when Ca 2+ was removed from the extracellular media, suggesting a role for the plasma membrane Na + /Ca 2+ exchanger (NCX). To further define a role for the NCX on CTGF formation we used dichlorobenzamil (DCB) and KB-R7943, two specific NCX inhibitors. DCB completely blocked the activation of B 1 receptor induced increase in CTGF mRNA stability while not affecting basal CTGF mRNA levels. In contrast, preincubation with EIPA, an amiloride analog, did not affect basal or stimulated CTGF mRNA levels. Furthermore, 60μM KB-R7943 blocked the B 1 stimulated rise in Ca cyt . NCX isoform 1 was identified in these cells using RT-PCR and immuno-detection. Thus, B 1 receptor stimulation increases fibrogenesis through a mechanism that involves modulation of cation metabolism via reverse-mode activation of NCX.

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Chen, Chung-Ming, Hsiu-Chu Chou, Leng-Fang Wang, and Yaw-Dong Lang. "Experimental Oligohydramnios Decreases Collagen in Hypoplastic Fetal Rat Lungs." Experimental Biology and Medicine 233, no. 11 (November 2008): 1334–40. http://dx.doi.org/10.3181/0803-rm-99.

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Neonates with premature rupture of the membrane and oligohydramnios have an increased risk of acute respiratory morbidity. The aims of this study are to investigate the effects of experimental oligohydramnios on transforming growth factor (TGF)-β1 and connective tissue growth factor (CTGF) expressions and collagen level in fetal rat lungs. On day 16 of gestation, we anesthetized timed pregnant Sprague-Dawley dams, punctured the uterine wall and fetal membranes of each amniotic sac which resulted in oligohydramnios. Fetuses in the opposite uterine horn served as controls. On days 19 and 21 of gestation, fetuses were delivered by cesarean section. Rats exposed to oligohydramnios exhibited significantly lower lung weight/body weight ratios on days 19 and 21 of gestation than did the control rats. Lung type I collagen and TGF-β1 mRNA expressions and lung collagen levels were significantly decreased in rats exposed to oligohydramnios on days 19 and 21 of gestation. Type I collagen and inhibitors of metalloproteinase-1 (TIMP-1) proteins were decreased and matrix metalloproteinase-1 (MMP-1) was increased in oligohydramnios-exposed rats on days 19 and 21 of gestation. CTGF mRNA expressions were comparable between control and oligohydramnios-exposed rats on days 19 and 21 of gestation. These data suggest that downregulation of collagen might be involved in the pathogenesis of oligohydramnios-induced respiratory morbidity.

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Wang, Shinong, and Raimund Hirschberg. "BMP7 antagonizes TGF-β-dependent fibrogenesis in mesangial cells." American Journal of Physiology-Renal Physiology 284, no. 5 (May 1, 2003): F1006—F1013. http://dx.doi.org/10.1152/ajprenal.00382.2002.

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Exogenous administration of recombinant human bone morphogenetic protein (BMP)-7 was recently shown to ameliorate renal glomerular and interstitial fibrosis in rodents with experimental renal diseases. We tested the hypothesis that BMP7 functions by antagonizing profibrogenic events that are induced by transforming growth factor (TGF)-β in cultured mesangial cells. Incubation of murine mesangial cells with TGF-β (50–200 pM) increased cell-associated collagen type IV and fibronectin, soluble collagen type IV, thrombospondin, and connective tissue growth factor (CTGF). Coincubation with recombinant human BMP7 (200 pM) reduced the increase of these ECM proteins and CTGF. The changes in collagen type IV and fibronectin proteins occurred without concomitant changes in collagen type α1IV and fibronectin mRNA levels, suggesting that TGF-β and BMP7 act primarily by affecting ECM protein degradation. Indeed, TGF-β decreases the levels and activity of matrix metalloprotease (MMP)-2, the major metalloprotease that is secreted by mesangial cells. Moreover, BMP7 inhibits TGF-β-induced activation of MMP2. Because TGF-β reduces the activity of MMPs through increasing plasminogen activator inhibitor (PAI)-1, we tested whether BMP7 interferes with this TGF-β effect. BMP7 reduces, by about two-thirds, the activation of a PAI-1 promoter/luciferase reporter in cells stably transfected with this construct. The findings from these studies indicate that BMP7 reduces TGF-β-induced ECM protein accumulation in cultured mesangial cells primarily by maintaining levels and activity of MMP2 partially through prevention of TGF-β-dependent upregulation of PAI-1.

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Hillege, Michèle, Ricardo Galli Caro, Carla Offringa, Gerard de Wit, Richard Jaspers, and Willem Hoogaars. "TGF-β Regulates Collagen Type I Expression in Myoblasts and Myotubes via Transient Ctgf and Fgf-2 Expression." Cells 9, no. 2 (February 6, 2020): 375. http://dx.doi.org/10.3390/cells9020375.

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Transforming Growth Factor β (TGF-β) is involved in fibrosis as well as the regulation of muscle mass, and contributes to the progressive pathology of muscle wasting disorders. However, little is known regarding the time-dependent signalling of TGF-β in myoblasts and myotubes, as well as how TGF-β affects collagen type I expression and the phenotypes of these cells. Here, we assessed effects of TGF-β on gene expression in C2C12 myoblasts and myotubes after 1, 3, 9, 24 and 48 h treatment. In myoblasts, various myogenic genes were repressed after 9, 24 and 48 h, while in myotubes only a reduction in Myh3 expression was observed. In both myoblasts and myotubes, TGF-β acutely induced the expression of a subset of genes involved in fibrosis, such as Ctgf and Fgf-2, which was subsequently followed by increased expression of Col1a1. Knockdown of Ctgf and Fgf-2 resulted in a lower Col1a1 expression level. Furthermore, the effects of TGF-β on myogenic and fibrotic gene expression were more pronounced than those of myostatin, and knockdown of TGF-β type I receptor Tgfbr1, but not receptor Acvr1b, resulted in a reduction in Ctgf and Col1a1 expression. These results indicate that, during muscle regeneration, TGF-β induces fibrosis via Tgfbr1 by stimulating the autocrine signalling of Ctgf and Fgf-2.

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Chaqour, Brahim, Catherine Whitbeck, Ji-Soo Han, Edward Macarak, Pat Horan, Paul Chichester, and Robert Levin. "Cyr61 and CTGF are molecular markers of bladder wall remodeling after outlet obstruction." American Journal of Physiology-Endocrinology and Metabolism 283, no. 4 (October 1, 2002): E765—E774. http://dx.doi.org/10.1152/ajpendo.00131.2002.

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Cysteine-rich protein (Cyr61) and connective tissue growth factor (CTGF) are key immediate early growth factors with functions in cell proliferation, differentiation, and extracellular matrix synthesis. Studies were performed to assess the gene expression profile of Cyr61 and CTGF in rat urinary bladder during growth in response to partial outlet obstruction. The mRNA levels of Cyr61 as determined by ribonuclease protection assay increased sharply after 1 day and remained elevated throughout the time period of the obstruction. This correlates well with increased bladder weight. The CTGF mRNA levels seemed to peak within the second week of the urethral obstruction and correlate well with increased type I collagen mRNA. The expression pattern of either Cyr61 or CTGF proteins corroborated that of their respective mRNAs. Immunohistochemical analyses showed that immunoreactivity of Cyr61 was confined to detrusor smooth muscle and that of CTGF was detected within both detrusor muscle and lamina propria layers. These data strongly indicate the involvement of Cyr61 and CTGF in bladder wall remodeling as a result of the outlet obstruction.

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Zhang, Lin, Jin Tan, Yi-Ping Liu, Xun Liu, and Mang Luo. "Curcumin relieves the arecoline-induced fibrosis of oral mucosal fibroblasts via inhibiting HIF-1α/TGF-β/CTGF signaling pathway: an in vitro study." Toxicology Research 10, no. 3 (May 2021): 631–38. http://dx.doi.org/10.1093/toxres/tfab046.

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Abstract Oral submacosal fibrosis (OSF) has been recognized as one of the oral potentially malignant disorders. Areca nut chewing is implicated in this pathological fibrosis. The current treatments for OSF have failed to achieve the desired curative effect. Here, we propose that curcumin has excellent therapeutic effect on OSF and explore its specific mechanism. Transwell assay was performed to detected cell migration. Flow cytometry was used to measured apoptosis. And MTT assay was performed to test cell viability. Gene and protein levels were detected by quantitative real-time polymerase chain reaction (qPCR) and western blotting. Our results displayed that curcumin treatment reduced fibrosis-related molecules (collagen type I alpha 1, collagen type III alpha 1, tissue inhibitor of metalloprotease 2) in arecoline-treated oral mucosal fibroblasts and elevated matrix metalloproteinase 2 expression. Additionally, curcumin could suppress cell proliferation and migration, and enhance the apoptosis of arecoline-treated normal oral mucosal fibroblasts. Most importantly, the hypoxia-inducible factor-1α (HIF-1α), transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF) expressions in arecoline-treated normal oral mucosal fibroblasts were reduced after exposure to curcumin, whereas the activation of HIF-1α/TGF-β/CTGF axis reversed curcumin’s effect on improving fibrosis of arecoline-treated normal oral mucosal fibroblasts. Therefore, curcumin alleviated oral submucosal fibrosis via inhibiting HIF-1α/TGF-β/CTGF axis. In summary, curcumin effectively inhibited the migration and proliferation and promoted apoptosis in arecoline-induced normal oral mucosal fibroblasts by inactivating HIF-1α/TGF-β/CTGF pathway. And curcumin might be a potential therapeutic drug for OSF treatment.

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McDonald, Emily A., Ling Cheng, Blanca Jarilla, Marianne J. Sagliba, Annaliza Gonzal, Amabelle J. Amoylen, Remigio Olveda, et al. "Maternal Infection with Schistosoma japonicum Induces a Profibrotic Response in Neonates." Infection and Immunity 82, no. 1 (October 28, 2013): 350–55. http://dx.doi.org/10.1128/iai.01060-13.

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ABSTRACTThe global burden of schistosomiasis is significant, with fibrosis a major associated morbidity and the primary cause of mortality. We have previously shown that schistosomiasis during pregnancy upregulates proinflammatory cytokines in the cord blood. In this study, we extend these findings to include a large panel of fibrosis-associated markers. We developed a multiplex bead-based assay to measure the levels of 35 proteins associated with fibrosis. Cord blood from 109 neonates born to mothers residing in an area ofSchistosoma japonicumendemicity was assessed for these molecules. Ten mediators were elevated in the cord blood from schistosome-infected pregnancies, including insulin-like growth factor 1 (IGF-1), tumor growth factor β1 (TGF-β1), connective tissue growth factor (CTGF), procollagen I carboxy-terminal propeptide (PICP), amino-telopeptide of type 1 collagen (ICTP), collagen VI, desmosine, matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinases 1 (TIMP-1), and TIMP-4. Many of these were also positively correlated with preterm birth (PICP, ICTP, MMP-2, TGF-β1, desmosine, CTGF, TIMP-1). In addition, birth weight was 168 g lower for infants with detectable levels of CTGF than for those with CTGF levels below the level of detection. Maternal schistosomiasis results in upregulation of fibrosis-associated proteins in the cord blood of the neonate, a subset of which are also associated with adverse birth outcomes. As the first report of fibrosis-associated molecules altered in the newborn of infected mothers, this study has broad implications for the health of the fetus, stretching from gestation to adulthood.

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Roestenberg, Peggy, Frans A. van Nieuwenhoven, Jaap A. Joles, Claudia Trischberger, Paula P. Martens, Noelynn Oliver, Jan Aten, Jo W. Höppener, and Roel Goldschmeding. "Temporal expression profile and distribution pattern indicate a role of connective tissue growth factor (CTGF/CCN-2) in diabetic nephropathy in mice." American Journal of Physiology-Renal Physiology 290, no. 6 (June 2006): F1344—F1354. http://dx.doi.org/10.1152/ajprenal.00174.2005.

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Connective tissue growth factor (CTGF) is overexpressed in diabetic nephropathy (DN) and has therefore been implicated in its pathogenesis. The objective of the present study was to determine the tissue distribution of increased CTGF expression and the relationship of plasma, urinary, and renal CTGF levels to the development and severity of DN. We studied the relationship between CTGF and renal pathology in streptozotocin (STZ)-induced diabetes in C57BL/6J mice. Diabetic and age-matched control mice were killed after 1, 2, 4, and 9 wk of diabetes. In addition, key parameters of diabetes and DN were analyzed in 10-mo-old diabetic ob/ob mice and their ob/+ littermates. STZ-induced diabetic mice showed a significantly increased urinary albumin excretion after 1 wk and increased mesangial matrix score after 2 wk. Increased renal fibronectin, fibronectin ED-A, and collagen IVα1 expression, as well as elevated plasma creatinine levels, were observed after 9 wk. After 2 wk, CTGF mRNA was upregulated threefold in the renal cortex. By 9 wk, CTGF mRNA was also increased in the heart and liver. In contrast, transforming growth factor-β1 mRNA content was significantly increased only in the kidney by 9 wk. Renal CTGF expression was mainly localized in podocytes and parietal glomerular epithelial cells, and less prominent in mesangial cells. In addition, plasma CTGF levels and urinary CTGF excretion were increased in diabetic mice. Moreover, albuminuria strongly correlated with urinary CTGF excretion ( R = 0.83, P < 0.0001). Increased CTGF expression was also demonstrated in type 2 diabetic ob/ob mice, which points to a causal relationship between diabetes and CTGF and thus argues against a role of STZ in this process. The observed relationship of podocyte and urinary CTGF to markers of DN suggests a pathogenic role of CTGF in the development of DN.

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Ploeg, Meike C., Chantal Munts, Tayeba Seddiqi, Tim J. L. ten Brink, Jonathan Breemhaar, Lorenzo Moroni, Frits W. Prinzen, and Frans A. van Nieuwenhoven. "Culturing of Cardiac Fibroblasts in Engineered Heart Matrix Reduces Myofibroblast Differentiation but Maintains Their Response to Cyclic Stretch and Transforming Growth Factor β1." Bioengineering 9, no. 10 (October 14, 2022): 551. http://dx.doi.org/10.3390/bioengineering9100551.

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Isolation and culturing of cardiac fibroblasts (CF) induces rapid differentiation toward a myofibroblast phenotype, which is partly mediated by the high substrate stiffness of the culture plates. In the present study, a 3D model of Engineered Heart Matrix (EHM) of physiological stiffness (Youngs modulus ~15 kPa) was developed using primary adult rat CF and a natural hydrogel collagen type 1 matrix. CF were equally distributed, viable and quiescent for at least 13 days in EHM and the baseline gene expression of myofibroblast-markers alfa-smooth muscle actin (Acta2), and connective tissue growth factor (Ctgf) was significantly lower, compared to CF cultured in 2D monolayers. CF baseline gene expression of transforming growth factor-beta1 (Tgfβ1) and brain natriuretic peptide (Nppb) was higher in EHM-fibers compared to the monolayers. EHM stimulation by 10% cyclic stretch (1 Hz) increased the gene expression of Nppb (3.0-fold), Ctgf (2.1-fold) and Tgfβ1 (2.3-fold) after 24 h. Stimulation of EHM with TGFβ1 (1 ng/mL, 24 h) induced Tgfβ1 (1.6-fold) and Ctgf (1.6-fold). In conclusion, culturing CF in EHM of physiological stiffness reduced myofibroblast marker gene expression, while the CF response to stretch or TGFβ1 was maintained, indicating that our novel EHM structure provides a good physiological model to study CF function and myofibroblast differentiation.

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Dissertations / Theses on the topic "Collagen Type 1 CTGF"

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Zhou, Zhenqing. "BIOLOGICAL SIGNIFICANCE OF HEPARIN-BINDING GROWTH FACTORS HB-EGF AND CTGF." Miami University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=miami1258498601.

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Mackay, Katrina. "Molecular analysis of type 1 collagen genes in inherited disorders." Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/34442.

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The collagens are a family of related proteins which contain at least one triple-helical domain, a structure which is determined by the unique amino acid sequence of the polypeptide subunits. These proteins each have a specific function in the extracellullar matrices of connective tissues of multicellular organisms. In humans, type I collagen, the most abundant collagen type, is the major structural component of skin, tendon and bone. Mutations in the two genes encoding the subunits of type I collagen, COL1A1 and COL1A2, result in heterogeneous phenotypes. Some mutations result in osteogenesis imperfecta, the "brittle bone disorder", which itself has a wide range of phenotypes from mild to lethal in utero and others result in Ehlers-Danlos syndrome type VII, which is characterized by skin hyperextensibility and joint laxity. In this study, mutations were detected in these two genes using an adaptation of a recently-developed technique, single strand conformation polymorphism analysis, and DNA sequencing. Several silent changes in COL1A1 were identified and characterized. Two of these, an intronic HaeIII restriction fragment length polymorphism and an AciI polymorphism, are both of sufficient frequency to be potentially useful as markers in linkage analysis studies. The AciI polymorphism, resulting in substitution of an alanine residue with threonine, and a proline to alanine change were both found in normal individuals and therefore the altered amino acid residues do not appear to have any crucial role in the type I collagen molecule. Four patients with Ehlers-Danlos syndrome were studied but no mutations were identified. Several different mutations, assumed to result in the disorder, were found in coding sequences of COL1A1 or COL1A2 in patients with lethal and non-lethal forms of osteogenesis imperfecta. The discovery of these mutations has extended the knowledge of the relationship between the type and position of the mutation and the resulting phenotype.

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Tang, Ming. "Atomic-scale biophysics modelling of type I collagen in the extracellular matrix." Thesis, Queensland University of Technology, 2019. https://eprints.qut.edu.au/124650/1/Ming_Tang_Thesis.pdf.

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This thesis explores the biophysics of collagen in the extracellular matrix under external stimuli, by performing cutting edge MD simulations. The obtained results provide significant insights into the design and manufacturing of artificial biomaterials for surgical tissue treatments, of collagen for regenerative medicine applications, and of gold nanoparticles for biomedical applications. The probed biophysical properties consist of the structural properties and the mechanical properties, where the mechanical properties of collagen are regulated by its structure at different levels of hierarchies.

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Dzobo, Kevin. "Matrix-mediated regulation of type 1 collagen synthesis and degradation in cultured fibroblasts." Doctoral thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/3125.

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Includes abstract.
Includes bibliographical references (leaves 122-157).
Stromal cells and the extracellular matrix (ECM) components provide the microenvironment that is pivotal for cell growth, motility, attachment and differentiation. Fibroblasts are some of the cells responsible for the synthesis of most of the extracellular matrix proteins. Type I collagen is the most abundant extracellular matrix protein in the human body and is found in tissues requiring high tensile strength. In this study we investigated the effect of a pre-formed fibroblast-derived extracellular matrix on the expression of type I collagen and associated matrix metalloproteinases in fibroblasts.

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Soininen, Raija. "Structure of the gene for the [alpha] 1 chain of human type IV collagen." Oulu, Finland : University of Oulu, 1989. http://catalog.hathitrust.org/api/volumes/oclc/20482376.html.

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Seehra, Kamaljit Jyoti Kaur. "An investigation into mechanisms inhibiting human microvascular endothelial cell (HMEC-1) capillary cord formation on collagen type 1." Thesis, University of Nottingham, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438638.

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Стужук, Анастасія Юріївна. "Способи отримання та перспективи застосування колагену типу 1." Магістерська робота, Київський національний університет технологій та дизайну, 2021. https://er.knutd.edu.ua/handle/123456789/19255.

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Дипломна магістерська робота присвячена вивченню способів отримання та перспектив застосування колагену типу 1 у різних галузях промисловості. У роботі наведено критичний огляд літературних джерел, присвячених застосуванню та отриманню колагену, обґрунтовано технологічну схему отримання сухого препарату колагену з відходів шкіряного виробництва за допомогою Bacillus subtilis, яка передбачає, в тому числі, стадії отримання посівного матеріалу, вирощування культури та культивування, поділ отриманого гідролізату на фракції та фільтрацію. Обґрунтовано вибір технологічного обладнання для реалізації виробництва. Дипломна робота включає біотехнологічні аспекти отримання колагену типу 1 та опис методів контролю стадій його виробництва та готового продукту.
The master's thesis is devoted to the study of methods of obtaining and prospects for the use of collagen type 1 in various industries. The thesis provides a critical review of the literature on the usage and production of collagen, substantiates the technological scheme of obtaining of a dry preparation of collagen from leather waste using Bacillus subtilis, which includes, inter alia, stages of seed production, cultivation, separation of hydrolyzate on fractions and filtration. The choice of technological equipment for the realization of production is substantiated. Thesis includes biotechnological aspects of obtaining of collagen type land a description of methods for controlling the stages of its production and finished product.

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Miles, Benjamin Nicholas. "On the use of collagen type-I in the growth of hydroxyapatite on micro-fabricated biomimetic dentin." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/58203.

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Dentin hypersensitivity is a condition that affects 4 – 14% of western populations like the U.K. It is characterised by a short sharp pain in the gums, usually experienced when an individual consumes cold food or drink. Typical treatments that are primarily delivered by sensitive toothpastes initially relied upon disruption of neuronal activity with potassium ions. However, more recently the most advanced over the counter treatments now act to occlude the tubules present in dentin that are involved in the hydrodynamic cause of dentinal pain. Pre-clinically, the efficacy of these occlusive treatments are assessed in a hydraulic conductance apparatus. This apparatus forces a simulated saliva through a thin section of dentin known as a Pashley dentin disc to determine a volumetric flow rate before and after treatment with the active of interest. Due to the innate variability of dentin a high degree of variability makes the assessment of novel actives difficult and unreliable. This body of work covers the attempt to fabricate a synthetic dentin disc that replicates the microstructure of the dentin and its tubules and in addition, the surface chemistry of the collagen and hydroxyapatite composite observed in dentin in vivo. The focus of this thesis is largely on the exploration of using collagen immobilised at the surface of this silicon mimetic dentin disc to template the growth of hydroxyapatite via a biomineralisation-like processes. An automated perfusion apparatus is used in attempt to mineralise a collagen coated mimetic dentin disc under conditions of continuous flow. A study of this flow mineralisation process over time was undertaken largely by Scanning Electron Microscopy. Whilst deposition of material was achieved at the mimetic dentin surface the full composition and morphology remained inconclusive however this work made significant headway into highlighting suitable routes forward in terms of fabrication and characterisation.

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Afifi, Amal. "A molecular investigation into type 1 collagen genes in Osteogenesis imperfecta and an evaluation of targeted gene repair." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422178.

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Ndlovu, Matladi N. "The role of DNA methylation in transcriptional regulation of the human type 1 alpha 2 collagen (COL1A2) gene." Master's thesis, University of Cape Town, 2002. http://hdl.handle.net/11427/3144.

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Bibliography leaves 70-97.
Type I collagen is the most abundant collagen molecule in vertebrate connective tissue and it consists of a heterotrimer of two alpha 1 (COL1A1) and one alpha 2 (COL1A2) chains. Reduced collagen gene expression is almost always correlated with pathological conditions and cellular transformation. Numerous studies have suggested that methylation of the cytosines in CpG dinucleotides is inversely correlated with transcriptional activity and plays a critical role in differential gene expression.

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Books on the topic "Collagen Type 1 CTGF"

1

Lee, Hyejin (Rosa). Critical role of membrane-type 1 matrix metalloproteinase in collagen phagocytosis by fibroblasts. 2007.

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2

Heidet, Laurence, Bertrand Knebelmann, and Marie Claire Gubler. Alport syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0321.

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Alport syndrome is an inherited renal disorder characterized by early haematuria, progressing to proteinuria, sensorineural hearing loss, and progressive renal failure typically in the third or fourth decade but with wide variation. It is responsible for about 1% of end-stage renal failure. Over 80% of cases are X-linked and young men are most affected, but heterozygous carriers of the abnormal gene are also at significantly increased risk of end-stage renal failure in their lifetime. Those affected by the autosomal recessive variant are phenotypically very similar. It is caused by mutations in tissue-specific isoforms of basement membrane (type IV) collagen encoded by COL4A5 (X chromosome), COL4A3, and COL4A4 (chromosome 2).

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DeAugustinas, M., and A. Kiely. Infectious Keratitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0016.

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Keratitis is an inflammation of the cornea, which can lead to corneal opacification or ulceration. The most common cause of infectious keratitis is herpes simplex virus type 1 (HSV-1). Noninfectious corneal infiltrates related to trauma, collagen vascular disease, autoimmune inflammation, vasculitis, or atopy (which predisposes to HSV keratitis) must be considered. HSV-associated stromal keratitis is the most common cause of infectious corneal blindness in the United States, yet its presentation can be fairly subtle. For this reason, symptoms out of proportion to exam findings or a history concerning for viral infection is an indication for prompt referral to ophthalmology. Topical antibiotic drops achieve high tissue concentrations and are the treatment of choice. Empiric coverage should be prescribed and tailored later under the care of an ophthalmologist. Other keys to effective treatment include discontinuing contact lens use and protecting the eye with a rigid shield without a patch, as patching provides a reservoir for infection.

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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0075.

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Alport antiglomerular basement membrane (anti-GBM) disease is a rare example of disease caused by allo-sensitization after renal transplantation, first described in 1992. Because the recipient lacks a specific glomerular basement membrane (GBM) protein, they can become sensitized to the normal molecule present in the GBM of the donor kidney. The disease is restricted to the allograft. Interestingly severe disease arises from this only arises rarely, certainly less than 1 in 20, probably closer to 1 in 50. It characteristically causes late graft loss in a first transplant with accelerated tempo in later allografts, and in its most extreme form recurs within days. However, inexplicably some subsequent transplants do not provoke aggressive recurrence. Treatment of the most aggressive disease is difficult and in most cases has been ultimately unsuccessful. Lower levels of immune response, marked by linear binding of immunoglobulin-G to GBM without glomerular disease, are not uncommon in Alport patients after transplantation and should not lead to altered treatment. Immunoassays for anti-GBM antibodies can be misleading as in most cases the target of antibodies is the α‎‎‎5 chain of type IV collagen, rather than the α‎‎‎3 chain which is the target in spontaneous anti-GBM disease. Overall the outcome of transplantation in Alport syndrome is better than average. This complication is more likely in patients with partial or total gene deletion rather than point mutations, but no other predictive features have been identified.

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Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

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Book chapters on the topic "Collagen Type 1 CTGF"

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Yamauchi, Mitsuo, Marnisa Sricholpech, Masahiko Terajima, Kenneth B. Tomer, and Irina Perdivara. "Glycosylation of Type I Collagen." In Post-Translational Modification of Proteins, 127–44. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9055-9_9.

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Ralston, Stuart H. "Type I Collagen Polymorphisms and Osteoporosis." In The Genetics of Osteoporosis and Metabolic Bone Disease, 61–74. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-033-9_4.

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Rittié, Laure. "Type I Collagen Purification from Rat Tail Tendons." In Fibrosis, 287–308. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_19.

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Rishikof, David C., Ping-Ping Kuang, Mangalalaxmy Subramanian, and Ronald H. Goldstein. "Methods for Measuring Type I Collagen Synthesis In Vitro." In Fibrosis Research, 129–40. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-940-0:129.

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Massimini, Marcella, Mariarita Romanucci, Raffaella De Maria, and Leonardo Della Salda. "Histological Evaluation of Long-Term Collagen Type I Culture." In Methods in Molecular Biology, 95–105. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2403-6_10.

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De Wever, Olivier, An Hendrix, Astrid De Boeck, Frank Eertmans, Wendy Westbroek, Geert Braems, and Marc E. Bracke. "Single Cell and Spheroid Collagen Type I Invasion Assay." In Methods in Molecular Biology, 13–35. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8244-4_2.

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Liu, Anjun, Hui Zhang, Ying Chen, Hongshuo Chen, Huihui Liu, and Xiaodan Guo. "Anti-Arthritic Effects of Chondroitin Sulfate and Type II Collagen in Collagen-Induced Arthritis Mice." In Lecture Notes in Electrical Engineering, 773–79. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4802-9_102.

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Yao, Shasha, Yifei Xu, Changyu Shao, Fabio Nudelman, Nico A. J. M. Sommerdijk, and Ruikang Tang. "A Biomimetic Model for Mineralization of Type-I Collagen Fibrils." In Methods in Molecular Biology, 39–54. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9095-5_4.

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Massimini, Marcella, Mariarita Romanucci, Raffaella De Maria, and Leonardo Della Salda. "Correction to: Histological Evaluation of Long-Term Collagen Type I Culture." In Methods in Molecular Biology, C1. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2403-6_17.

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Harris, J. Robin. "Visualizing In Vitro Type I Collagen Fibrillogenesis by Transmission Electron Microscopy." In Fibrosis, 367–83. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_24.

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Conference papers on the topic "Collagen Type 1 CTGF"

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Juncosa-Melvin, Natalia, Karl S. Matlin, Robert W. Holdcraft, Victor S. Nirmalanandhan, and David L. Butler. "Mechanical Stimulation Increases Collagen Type I and Collagen Type III Gene Expression of Stem Cell: Collagen Sponge Constructs for Patellar Tendon Repair." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175807.

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Tendons (rotator cuff, Achilles and patellar tendons) are among the most commonly injured soft tissues [1]. Many repairs/reconstructions have been attempted using sutures, resorbable biomaterials, autografts, and allografts, but with varying success. A tissue engineered repair using mesenchymal stem cells (MSCs) is attractive [2–4] but often lacks initial stiffness and strength [5].

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Gaudet, Ian D., and David I. Shreiber. "Photocrosslinkable Type-I Collagen for In Situ Material Modification." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53125.

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Hydrogels are attractive materials for use as tissue engineering scaffolds [1]. Natural hydrogels, such as collagen, are both cytocompatible and highly biofunctional. However, they have somewhat constrained material properties and have an inherently large variability in composition due to their biological origin, making them more difficult to work with from an engineering viewpoint[2–4]. Here, we aim to use type 1 collagen — the most abundant protein in the body that maintains excellent cytocompatibility and can self assemble into a fibrillar network — as a base component for a photocrosslinkable biomaterial. One main advantage of this system over previous studies attempting to photocrosslink collagen is that the collagen retains its ability to self assemble, which provides a stable environment into which localized modifications can be made to the stiffness, porosity, and biochemical properties of the hydrogel scaffold. By taking advantage of the spatial control provided by the system, we can create complex 3-dimensional hydrogel scaffolds that have non-homogenous microenvironments.

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Gyoneva, Lazarina, Mohammad F. Hadi, Yoav Segal, Kevin D. Dorfman, and Victor H. Barocas. "Role of Lateral Interactions in Type IV Collagen Network Mechanics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14625.

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The basement membrane is a specialized part of the extra-cellular matrix. It is usually characterized as a scaffold for epithelial cells but in some tissues it serves other, mechanical, roles [1]. The mechanical properties of the basement membrane are mainly determined by one of its main constituents — type IV collagen. Unlike the well-known fibrous type I collagen, collagen IV assembles into planar networks (Fig. 1) [2]. The α 1(IV) and α 2(IV) collagen IV chains assemble into the so-called major chain network, present in all basement membranes. The α 3(IV), α 4(IV), α 5(IV) collagen IV chains form the minor chain network which is found only in the adult basement membranes of the kidney glomerular capillaries (GBM), ocular lens (LBM), cochlea, and the testes [3]. The minor chains have a higher number of cysteine residues, allowing them to form a higher number of lateral interactions. In the minor chain network, the greater potential to interact laterally manifests in the formation of super-coils, which are rarely observed in the major chain network [4]. Increasing the number of cross-links in a polymeric material is known to increase material stiffness; therefore, it is believed that the minor chain network confers basement membranes with additional strength and stability [5]. In the hereditary disease Alport syndrome, a mutation causes the absence of the minor chain network. The GBM and LBM of Alport patients appear weakened and unable to meet their mechanical demands, further supporting this theory [6]. The objective of this study was to evaluate the importance of cross-linking in the minor chains for the mechanical properties of type IV collagen networks, specifically in the GBM and LBM where the absence of the minor chains has an observed mechanical effect.

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Schuliga, Michael, Trudi Harris, and Alastair Stewart. "Plasmin Formation By Airway Smooth Muscle Is Accelerated By Culture On Fibrillar Type 1 Collagen." 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.a2078.

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Gee, Albert O., Brendon M. Baker, and Robert L. Mauck. "Mechanics and Cytocompatibility of Genipin Crosslinked Type I Collagen Nanofibrous Scaffolds." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193220.

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Collagen is a principal constituent of the extracellular matrix (ECM) and as such, defines the microenvironmental milieu in which cells reside. In fiber-reinforced musculoskeletal tissues, collagen fibers are highly organized and generate the direction-dependent mechanical properties critical to the function of these structures. Given its primary role, collagen is particularly attractive for tissue engineering (TE) applications where scaffolds are coupled with cells to repair or regenerate damaged tissues. One method for producing collagen-based scaffolds is through electrospinning. This technique yields nano- to micron-scale fibers similar in diameter to those of the native ECM. Towards engineering orthopaedic tissues, methods have been devised to electrospin fibers into aligned arrays that can recapitulate the anisotropy of fiber-reinforced tissues [1]. While a number of polymers have been electrospun, collagen-based scaffolds are especially promising as they provide a biomimetic interface for cell attachment [2]. Numerous investigators have electrospun collagen [3], one major drawback is their inherent instability in aqueous environments. To address this, various crosslinking agents including glutaraldehyde (GA), 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride, and N-hydroxysuccinimide chemistries have been used, but these chemicals often prove cytotoxic or excessively laborious in application [4]. Even with crosslinking, dry as-formed nanofibrous collagen scaffolds with moduli greater than 50MPa diminish by 100-fold with rehydration [5].

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Lai, Victor K., Allan M. Kerandi, Spencer P. Lake, Robert T. Tranquillo, and Victor H. Barocas. "Collagen Network Architecture Varies Between Pure Collagen and Collagen-Fibrin Co-Gels." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80738.

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Naturally-occurring extracellular matrix (ECM) proteins, e.g. collagen I and fibrin, play an important role in tissues, conferring structural integrity and providing a biochemical environment for eliciting important cellular responses (e.g. migration). Tissue engineers use a variety of matrix polymers as initial scaffolds for seeding cells, sometimes in combination with one another (e.g. collagen-fibrin [1]). For example, our group fabricates arterial tissue equivalents (TEs) by seeding cells in a fibrin gel, which is gradually degraded over time and replaced by cell-produced collagen [2]. While the structure and mechanics of individual ECM proteins have been studied extensively, how multiple fibrillar networks interact to confer overall mechanical behavior remains poorly understood. Narrowing this gap in knowledge of scaffolds comprising multiple fibril networks is crucial in allowing for more rational design in tissue engineering, as cells react differently according to their mechanical environments. For collagen-fibrin networks in particular, early efforts in elucidating interactions between these two fibril networks in co-gels have proven inconclusive due to inconsistent findings from various groups. Recent modeling efforts by our group have shown that simple “series” and “parallel” type interactions provide bounds for the mechanical behavior of collagen-fibrin co-gels [3]. In addition, experiments on pure collagen and fibrin vs. their respective networks from collagen-fibrin co-gels after digestion showed slight differences in mechanical behavior [4]. These previous studies have focused on the composition-function relationship between collagen and fibrin. The objective of the current work is to explore how collagen network architecture changes in the presence of the fibrin network in collagen-fibrin co-gels, thereby providing an added dimension to our understanding of collagen-fibrin systems by elucidating structure-composition-function relationships between collagen and fibrin.

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Lambert, C., D. Borderie, F. Rannou, and Y. Henrotin. "SAT0052 The coll2–1 peptide of collagen type ii: a new actor of synovitis in osteoarthritis." 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.1036.

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Rada, Miran, Catherine Eldred, Jessica Sage, Sandra Orsulic, and Dong-Joo Cheon. "Abstract TMEM-017: COLLAGEN TYPE XI ALPHA 1 (COL11A1) IS A NOVEL STROMAL MEDIATOR OF CHEMORESISTANCE." In Abstracts: 11th Biennial Ovarian Cancer Research Symposium; September 12-13, 2016; Seattle, WA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.ovcasymp16-tmem-017.

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Jensen, Christina, Anders Kverneland, Marco Donia, Neel I. Nissen, Morten A. Karsdal, Inge Marie Svane, and Nicholas Willumsen. "Abstract 388: Non-invasive biomarker potential of the fibroblast-derived collagen type III and collagen type XI for predicting outcome in metastatic melanoma patients treated with anti-PD-1 therapy." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-388.

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Ahmad Tantowi, Nur Adeelah Che, and Jemma Kerns. "THU0023 PARADOXICAL EFFECT OF INTERLEUKIN 1 BETA CYTOKINE ON COLLAGEN TYPE I SYNTHESIS IN OSTEOBLAST-LIKE CELLS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8291.

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