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1
Chiquet-Ehrismann, R., M. Tannheimer, M. Koch, et al. "Tenascin-C expression by fibroblasts is elevated in stressed collagen gels." Journal of Cell Biology 127, no. 6 (1994): 2093–101. http://dx.doi.org/10.1083/jcb.127.6.2093.
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Chick embryo fibroblasts cultured on a collagen matrix exert tractional forces leading to the contraction of unrestrained, floating collagen gels and to the development of tension in attached, restrained gels. On a restrained, attached collagen gel the fibroblasts synthesize large quantities of tenascin-C, whereas in a floating, contracting gel tenascin-C synthesis is decreased. This regulation of tenascin-C synthesis can be observed by the secretion of metabolically labeled tenascin-C into the conditioned medium, as well as by the deposition of tenascin-C into the collagen matrix as judged by immunofluorescence. Regulation appears to occur at the transcriptional level, because when cells on attached or floating collagen gels are transfected with promoter constructs of the tenascin-C gene, luciferase expression driven by the tenascin-C promoter parallels the effects measured for endogenous tenascin-C synthesis, whereas luciferase expression under the control of the SV40 promoter does not depend on the state of the collagen gel. The promoter region responsible for tenascin-C induction on attached collagen gels is distinct from the region important for the induction of tenascin-C by serum, and may define a novel kind of response element. By joining this tenascin-C sequence to the SV40 promoter of a reporter plasmid, its activity can be transferred to the heterologous promoter. We propose that the tenascin-C promoter is directly or indirectly activated in fibroblasts generating and experiencing mechanical stress within a restrained collagen matrix. This may be an important aspect of the regulation of tenascin-C expression during embryogenesis as well as during wound healing and other regenerative and morphogenetic processes.
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Talts, J. F., A. Weller, R. Timpl, M. Ekblom, and P. Ekblom. "Regulation of mesenchymal extracellular matrix protein synthesis by transforming growth factor-beta and glucocorticoids in tumor stroma." Journal of Cell Science 108, no. 6 (1995): 2153–62. http://dx.doi.org/10.1242/jcs.108.6.2153.
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We have here studied the composition and regulation of stromal extracellular matrix components in an experimental tumor model. Nude mice were inoculated with WCCS-1 cells, a human Wilms' tumor cell line. In the formed tumors the stroma was found to contain mesenchymal extracellular matrix proteins such as tenascin-C, fibulins-1 and 2 and fibronectin, but no nidogen. Nidogen was confined to basement membranes of tumor blood vessels. Since glucocorticoids have been shown to downregulate tenascin-C expression in vitro, we tested whether dexamethasone can influence biosynthesis of extracellular matrix components during tumor formation in vivo. A downregulation of tenascin-C mRNA and an upregulation of fibronectin mRNA expression by dexamethasone was noted. Transforming growth factor-beta 1 mRNA levels were unaffected by the dexamethasone treatment. Glucocorticoids can thus downregulate tenascin-C synthesis although local stimulatory growth factors are present. The competition between a negative and a positive extrinsic factor on synthesis of stromal extracellular matrix components was studied in a fibroblast/preadipocyte cell line. Transforming growth factor-beta 1 stimulated tenascin-C synthesis but did not affect fibronectin or fibulin-2 synthesis. Dexamethasone at high concentrations could completely suppress the effect of transforming growth factor-beta 1 on tenascin-C mRNA expression. Transforming growth factor-beta 1 could in turn overcome the downregulation of tenascin-C mRNA expression caused by a lower concentration of dexamethasone. We therefore suggest that the limited expression of tenascin-C in part is due to a continuous suppression by physiological levels of glucocorticoids, which can be overcome by local stimulatory growth factors when present in sufficient amounts.
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Jones, P. L., N. Boudreau, C. A. Myers, H. P. Erickson, and M. J. Bissell. "Tenascin-C inhibits extracellular matrix-dependent gene expression in mammary epithelial cells. Localization of active regions using recombinant tenascin fragments." Journal of Cell Science 108, no. 2 (1995): 519–27. http://dx.doi.org/10.1242/jcs.108.2.519.
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The physiological role of tenascin in vivo has remained obscure. Although tenascin is regulated in a stage and tissue-dependent manner, knock-out mice appear normal. When tenascin expression was examined in the normal adult mouse mammary gland, little or none was present during lactation, when epithelial cells actively synthesize and secrete milk proteins in an extracellular matrix/lactogenic hormone-dependent manner. In contrast, tenascin was prominently expressed during involution, a stage characterized by the degradation of the extracellular matrix and the subsequent loss of milk production. Studies with mammary cell lines indicated that tenascin expression was high on plastic, but was suppressed in the presence of the laminin-rich, Engelbreth-Holm-Swarm (EHS) tumour biomatrix. When exogenous tenascin was added together with EHS to mammary epithelial cells, beta-casein protein synthesis and steady-state mRNA levels were inhibited in a concentration-dependent manner. Moreover, this inhibition by tenascin could be segregated from its effects on cell morphology. Using two beta-casein promoter constructs attached to the chloramphenicol acetyltransferase reporter gene we showed that tenascin selectively suppressed extracellular matrix/prolactin-dependent transcription of the beta-casein gene in three-dimensional cultures. Finally, we mapped the active regions within the fibronectin type III repeat region of the tenascin molecule that are capable of inhibiting beta-casein protein synthesis. Our data are consistent with a model where both the loss of a laminin-rich basement membrane by extracellular matrix-degrading enzymes and the induction of tenascin contribute to the loss of tissue-specific gene expression and thus the involuting process.
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Jones, P. L., F. S. Jones, B. Zhou, and M. Rabinovitch. "Induction of vascular smooth muscle cell tenascin-C gene expression by denatured type I collagen is dependent upon a beta3 integrin-mediated mitogen-activated protein kinase pathway and a 122-base pair promoter element." Journal of Cell Science 112, no. 4 (1999): 435–45. http://dx.doi.org/10.1242/jcs.112.4.435.
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Tenascin-C is an extracellular matrix glycoprotein, the expression of which is upregulated in remodeling arteries. In previous studies we showed that the presence of tenascin-C alters vascular smooth muscle cell shape and amplifies their proliferative response by promoting growth factor receptor clustering and phosphorylation. Moreover, we demonstrated that denatured type I collagen induces smooth muscle cell tenascin-C protein production via beta3 integrins. In the present study, we examine the pathway by which beta3 integrins stimulate expression of tenascin-C, and define a promoter sequence that is critical for its induction. On native collagen, A10 smooth muscle cells adopt a stellate morphology and produce low levels of tenascin-C mRNA and protein, whereas on denatured collagen they spread extensively and produce high levels of tenascin-C mRNA and protein, which is incorporated into an elaborate extracellular matrix. Increased tenascin-C synthesis on denatured collagen is associated with elevated protein tyrosine phosphorylation, including activation of extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2). beta3 integrin function-blocking antibodies attenuate ERK1/2 activation and tenascin-C protein synthesis. Consistent with these findings, treatment with the specific MEK inhibitor, PD 98059, results in suppression of tenascin-C protein synthesis. To investigate whether beta3 integrin-dependent activation of ERK1/2 regulates the tenascin-C promoter, we transfected A10 cells with a full-length (approx. 4 kb) mouse tenascin-C gene promoter-chloramphenicol acetyltransferse reporter construct and showed that, relative to native collagen, its activity is increased on denatured collagen. Next, to identify regions of the promoter involved, we examined a series of tenascin-C promoter constructs with 5′ deletions and showed that denatured collagen-dependent promoter activity was retained by a 122-base pair element, located -43 to -165 bp upstream of the RNA start site. Activation of this element was suppressed either by blocking beta3 integrins, or by preventing ERK1/2 activation. These observations demonstrate that smooth muscle cell binding to beta3 integrins activates the mitogen activated protein kinase pathway, which is required for the induction of tenascin-C gene expression via a potential extracellular matrix response element in the tenascin-C gene promoter. Our data suggest a mechanism by which remodeling of type I collagen modulates tenascin-C gene expression via a beta3 integrin-mediated signaling pathway, and as such represents a paradigm for vascular development and disease whereby smooth muscle cells respond to perturbations in extracellular matrix composition by altering their phenotype and patterns of gene expression.
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Sakai, T., Y. Furukawa, R. Chiquet-Ehrismann, et al. "Tenascin-X expression in tumor cells and fibroblasts: glucocorticoids as negative regulators in fibroblasts." Journal of Cell Science 109, no. 8 (1996): 2069–77. http://dx.doi.org/10.1242/jcs.109.8.2069.
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Tenascin-X has recently been shown to be a novel member of the tenascin family and its distribution is often reciprocal to that of tenascin-C in the developing mouse embryo. We have investigated the expression of tenascin-X in fibroblasts and carcinoma cells in culture. Tenascin-X protein was secreted in vitro in the conditioned media at an apparent molecular mass of approximately 450 kDa. In addition fibroblasts contained a major tenascin-X isoform of 220 kDa. On northern blots, a single major transcript with a size of approximately 13 kb was detected. No overexpression of tenascin-X protein was found in primary fibroblasts of the tenascin-C-gene knockout mice. Steroid hormone glucocorticoids, were found to downregulate tenascin-X mRNA levels and protein synthesis in fibroblasts but not carcinoma cells at physiological concentrations. None of the growth factors or cytokines examined affected the expression level of tenascin-X. As in vivo study, carcinoma cells were transplanted into nude mice. In contrast to the ubiquitous presence of tenascin-X in adult skin, expression of tenascin-X protein during tumorigenesis was found to be down-regulated considerably not only in tumor cells themselves but also in tumor stroma. These findings provide evidence that the expression of tenascin-X can be influenced by stromal-epithelial interactions. We have identified glucocorticoids as physiological inhibitors of tenascin-X and suggest that glucocorticoids may in part participate in the downregulation of tenascin-X in fibroblasts in vivo.
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Riou, J. F., D. L. Shi, M. Chiquet, and J. C. Boucaut. "Expression of tenascin in response to neural induction in amphibian embryos." Development 104, no. 3 (1988): 511–24. http://dx.doi.org/10.1242/dev.104.3.511.
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The expression of tenascin, a constituent of extracellular matrix (ECM), was studied during the embryonic development of the amphibian Pleurodeles waltl. An antiserum to chick fibroblast tenascin was shown to cross-react with the homologous molecule of the amphibian. Immunostaining of embryo sections with anti-tenascin antiserum revealed that tenascin appears just after the completion of neurulation. At the tailbud stage, tenascin is present in the ECM located at sites of directed cell migration (neural crest cell migration pathways, extension of the pronephretic duct) and mesenchyme condensation (endocardium, aortic arches). The accumulation of tenascin immunoreactivity in the embryonic ECM is correlated with the synthesis of the 220×103Mr polypeptide of the molecule. To provide data on the patterning of tenascin, ectoderm and dorsal blastoporal lip isolated at early gastrula stage were cultured for a period of 3 days. Epidermal vesicles differentiating from isolated ectoderm completely lack tenascin. Conversely, axial mesoderm derivatives present in cultured dorsal blastoporal lip were found to produce tenascin. Neural induction of ectoderm isolated at early gastrula stage was performed in vitro with the dorsal blastoporal lip or concanavalin A. The induced neural tissue was found to accumulate tenascin. Spemann experiments confirmed in vivo that tenascin is expressed by ectodermal cells as a response to neural induction.
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Mackie, E. J., and S. Ramsey. "Modulation of osteoblast behaviour by tenascin." Journal of Cell Science 109, no. 6 (1996): 1597–604. http://dx.doi.org/10.1242/jcs.109.6.1597.
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The extracellular matrix protein tenascin is secreted by osteoblasts but absent from mineralized bone matrix. The current study was undertaken to test the hypothesis that tenascin regulates osteoblast behaviour. Three osteoblast-like cell lines UMR-106, ROS-17/2.8 (rat) and SAOS-2 (human) were used to investigate the role of tenascin in osteoblast morphology, differentiation and proliferation. Two of three cell lines adhered specifically to tenascin, remaining round and failing to spread. Tenascin as a substratum stimulated alkaline phosphatase activity (a marker of osteoblast differentiation) in two of three cell lines. Moreover, anti-tenascin in the medium caused a reduction in alkaline phosphatase levels in all three cell lines. Anti-tenascin also inhibited collagen synthesis, an important osteoblast function. Since it seemed possible that tenascin may exert its effects on cell function through its ability to cause cell rounding, the ability of cell shape change alone to influence alkaline phosphatase levels was investigated. Cells were incubated in the presence of cytochalasin D and alkaline phosphatase levels assayed. Alkaline phosphatase activity was not elevated by cytochalasin D treatment, indicating that cell rounding alone is insufficient to mimic the effect of tenascin. Anti-tenascin caused a slight increase in proliferation of SAOS-2 cells, indicating that tenascin is itself inhibitory. In ROS 17/2.8 and UMR-106 cells, in contrast, proliferation was inhibited by anti-tenascin. The results presented here indicate that tenascin is able to stimulate osteoblastic differentiation and that endogenous tenascin helps to maintain the functional state of cultured osteoblast-like cells.
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Lang, Stephan, Volker Schilling, Brigitte Mack, Barbara Wollenberg та Andreas Nerlich. "Localization of Transforming Growth Factor-β- Expressing Cells and Comparison with Major Extracellular Components in Aural Cholesteatoma". Annals of Otology, Rhinology & Laryngology 106, № 8 (1997): 669–73. http://dx.doi.org/10.1177/000348949710600810.
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Transforming growth factor-β (TGF-β) plays an important role in the regulation of extracellular matrix (ECM) deposition by stimulating the synthesis of individual matrix proteins like tenascin and fibronectin. Cholesteatoma shows significant changes in the ECM, supporting the view of adisturbed cell-matrix interaction. The purpose of our present study was to evaluate the distribution of TGF-β in comparison to the deposition of tenascin, fibronectin, and collagen as major components of the ECM in cholesteatoma (n = 12) by means of histochemistry and immunohistochemistry. We found TGF-P in lymphocytes and fibrohistiocytes in the stroma of 7 cholesteatomas. In corresponding sections, a marked expression of tenascin and fibronectin was seen manifesting as a continuous band along the epidermal-stromal junction, extending to the deeper stroma. In addition, in those cases of TGF-β expression, beginning collagen fibril formation was seen in adjacent deeper stroma layers, indicating beginning stromal fibrosis. These results suggest that TGF-β may be involved in the stimulation of the synthesis of tenascin, fibronectin, and collagen. Furthermore, the enhanced expression of tenascin and fibronectin provides evidence for a deregulated cell-matrix interaction in cholesteatoma associated with the enhanced proliferative process of cholesteatoma formation.
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Wirl, G., M. Hermann, P. Ekblom, and R. Fassler. "Mammary epithelial cell differentiation in vitro is regulated by an interplay of EGF action and tenascin-C downregulation." Journal of Cell Science 108, no. 6 (1995): 2445–56. http://dx.doi.org/10.1242/jcs.108.6.2445.
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Expression of the extracellular matrix glycoprotein tenascin-C in the mammary gland is associated with cellular proliferation and cell motility during organogenesis and tumorigenesis. Because the source and the regulation of tenascin-C in these tissues are unclear, we have used tenascin-C cDNA, FITC-immunofluorescence and immuno-precipitation to examine tenascin-C expression of mammary epithelial cells. Using several mammary epithelial cell lines we could show that tenascin-C can be produced and secreted by epithelial cells. However it was found that tenascin-C synthesis was inversely correlated with the polarized epithelial phenotype. Among three mouse mammary epithelial cell clones, tenascin-C expression was most abundant in HC-11 cells, the least differentiated cell type. Expression levels were high during the growth phase but were nearly abolished when cells were grown to confluence and induced to express milk proteins. Downregulation of tenascin-C by EGF apparently commits HC-11 cells to respond to lactogenic hormones and consequently, hormone induced levels of beta-casein mRNA decreased significantly when HC-11 cells were grown on a tenascin-C substrate. On the other hand, TGF-beta, another growth factor involved in coordinated growth and differentiation of the mammary gland in vivo was found to be a very potent inducer of tenascin-C. The generation of fully polarized and tight epithelium affected the levels of tenascin-C expression. In contrast to HC-11 cells, which do not form epithelial domes in vitro, highly polarized and dome forming EpH4 and Fos-ER cells nearly lacked tenascin-C. Similarly, induction of dome formation in the rat mammary stem cell line Rama 25 by the differentiation inducer dimethylsulfoxide caused a loss of TN-C-transcripts. The inability of Fos-ER cells to develop domes in the presence of soluble tenascin-C also suggests its interference with induction and maintenance of mammary epithelial cell differentiation.
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Gatchalian, C. L., M. Schachner, and J. R. Sanes. "Fibroblasts that proliferate near denervated synaptic sites in skeletal muscle synthesize the adhesive molecules tenascin(J1), N-CAM, fibronectin, and a heparan sulfate proteoglycan." Journal of Cell Biology 108, no. 5 (1989): 1873–90. http://dx.doi.org/10.1083/jcb.108.5.1873.
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Four adhesive molecules, tenascin(J1), N-CAM, fibronectin, and a heparan sulfate proteoglycan, accumulate in interstitial spaces near synaptic sites after denervation of rat skeletal muscle (Sanes, J. R., M. Schachner, and J. Covault. 1986. J. Cell Biol. 102:420-431). We have now asked which cells synthesize these molecules, and how this synthesis is regulated. Electron microscopy revealed that mononucleated cells selectively accumulate in perisynaptic interstitial spaces beginning 2 d after denervation. These cells were identified as fibroblasts by ultrastructural and immunohistochemical criteria; [3H]thymidine autoradiography revealed that their accumulation results from local proliferation. Electron microscopic immunohistochemistry demonstrated that N-CAM is associated with the surface of the fibroblasts, while tenascin(J1) is associated with collagen fibers that abut fibroblasts. Using immunofluorescence and immunoprecipitation methods, we found that fibroblasts isolated from perisynaptic regions of denervated muscle synthesize N-CAM, tenascin(J1), fibronectin, and a heparan sulfate proteoglycan in vitro. Thus, fibroblasts that selectively proliferate in interstitial spaces near synaptic sites are likely to be the cellular source of the interstitial deposits of adhesive molecules in denervated muscle. To elucidate factors that might regulate the accumulation of these molecules in vivo, we analyzed the expression of tenascin(J1) and fibronectin by cultured fibroblasts. Fibroblasts from synapse-free regions of denervated muscle, as well as skin, lung, and 3T3 fibroblasts accumulate high levels of tenascin(J1) and fibronectin in culture, showing that perisynaptic fibroblasts are not unique in this regard. However, when they are first placed in culture, fibroblasts from denervated muscle bear more tenascin(J1) than fibroblasts from innervated muscle, indicating that expression of this molecule by fibroblasts is regulated by the muscle's state of innervation; this difference is no longer apparent after a few days in culture. In 3T3 cells, accumulation of tenascin(J1) is high in proliferating cultures, depressed in confluent cultures, and reactivated in cells stimulated to proliferate by replating at low density or by wounding a confluent monolayer. Thus, synthesis of tenascin(J1) is regulated in parallel with mitotic activity. In contrast, levels of fibronectin, which increase less dramatically after denervation in vivo, are similar in fibroblasts from innervated and denervated muscle and in proliferating and quiescent 3T3 cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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Trebaul, A., E. K. Chan, and K. S. Midwood. "Regulation of fibroblast migration by tenascin-C." Biochemical Society Transactions 35, no. 4 (2007): 695–97. http://dx.doi.org/10.1042/bst0350695.
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Synthesis of new tissue by fibroblasts is required for tissue rebuilding in response to injury. Fibroblast migration from surrounding healthy tissue into the fibrin–fibronectin provisional matrix deposited upon injury is a key rate-limiting step of this stage of tissue repair. These events must be tightly regulated. Excessive deposition of scar tissue is the major hallmark of fibrotic disease. Tenascin-C is an extracellular matrix glycoprotein that is transiently expressed upon tissue injury, where it is specifically localized to the wound edge, and persistently up-regulated in fibrotic disease. We have shown that full-length tenascin-C promotes fibroblast migration within fibrin–fibronectin matrices and we have mapped the domains within the molecule critical for enhancing migration. We also demonstrated that specific fragments of tenascin-C inhibit fibroblast migration. These results suggest that transient expression of tenascin-C at the wound boundary is key to tissue repair: its induction recruits fibroblasts into the wound and fragments resulting from its breakdown prevent excessive fibroblast infiltration. Our results demonstrate how fibroblast migration in three-dimensional provisional matrices may be differentially regulated by proteolysis of matrix molecules and could explain how persistent expression of tenascin-C contributes to the progression of fibrotic disease.
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Woodworth, Alison, Penka Pesheva, Dorothy Fiete, and Jacques U. Baenziger. "Neuronal-specific Synthesis and Glycosylation of Tenascin-R." Journal of Biological Chemistry 279, no. 11 (2003): 10413–21. http://dx.doi.org/10.1074/jbc.m312466200.
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Mettouchi, A., F. Cabon, N. Montreau, et al. "The c-Jun-induced transformation process involves complex regulation of tenascin-C expression." Molecular and Cellular Biology 17, no. 6 (1997): 3202–9. http://dx.doi.org/10.1128/mcb.17.6.3202.
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In cooperation with an activated ras oncogene, the site-dependent AP-1 transcription factor c-Jun transforms primary rat embryo fibroblasts (REF). Although signal transduction pathways leading to activation of c-Jun proteins have been extensively studied, little is known about c-Jun cellular targets. We identified c-Jun-upregulated cDNA clones homologous to the tenascin-C gene by differential screening of a cDNA library from REF. This tightly regulated gene encodes a rare extracellular matrix protein involved in cell attachment and migration and in the control of cell growth. Transient overexpression of c-Jun induced tenascin-C expression in primary REF and in FR3T3, an established fibroblast cell line. Surprisingly, tenascin-C synthesis was repressed after stable transformation by c-Jun compared to that in the nontransformed parental cells. As assessed by using the tenascin-C (-220 to +79) promoter fragment cloned in a reporter construct, the c-Jun-induced transient activation is mediated by two binding sites: one GCN4/AP-1-like site, at position -146, and one NF-kappaB site, at position -210. Furthermore, as demonstrated by gel shift experiments and cotransfections of the reporter plasmid and expression vectors encoding the p65 subunit of NF-kappaB and c-Jun, the two transcription factors bind and synergistically transactivate the tenascin-C promoter. We previously described two other extracellular matrix proteins, SPARC and thrombospondin-1, as c-Jun targets. Thus, our results strongly suggest that the regulation of the extracellular matrix composition plays a central role in c-Jun-induced transformation.
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Canfield, A. E., and A. M. Schor. "Evidence that tenascin and thrombospondin-1 modulate sprouting of endothelial cells." Journal of Cell Science 108, no. 2 (1995): 797–809. http://dx.doi.org/10.1242/jcs.108.2.797.
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Cultured endothelial cells undergo a reversible transition from a resting (cobblestone) phenotype to an angiogenic (sprouting) phenotype. This transition mimics the early events of angiogenesis. We have previously reported that the addition of exogenous xylosides inhibits endothelial cel sprouting and modifies the extracellular matrix (ECM) synthesised by the cells. We have now investigated whether endothelial sprouting is mediated by the nature of the extracellular matrix in contact with the cells. Accordingly, cell-free matrices deposited by bovine aortic endothelial cells (BAEC) were isolated. These matrices were produced under conditions in which the formation of the sprouting phenotype was permitted (controls) or inhibited (by the addition of exogenous xylosides). BAEC were then plated on these matrices and grown under conditions which promote sprouting. Sprouting proceeded normally on control matrices, whereas it was inhibited when the cells were grown on matrices deposited in the presence of xylosides. The composition of the permissive and inhibitory matrices was then analysed. Inhibitory matrices contained reduced levels of tenascin and increased levels of thrombospondin-1 by comparison to the permissive matrices. In contrast, no differences were detected in the relative levels of laminin. The roles of tenascin and thrombospondin-1 in endothelial sprouting were confirmed using specific antibodies. Immunolocalisation studies revealed the presence of both proteins in sprouting cells. Antibodies to tenascin inhibited the formation of sprouting cells on permissive matrices and on gelatin-coated dishes without affecting cell growth. Tenascin synthesis was increased when sprouting cells were present in the cultures. Antibodies to thrombospondin-1 stimulated sprouting on inhibitory matrices. These results suggest that the transition from a resting to a sprouting phenotype is promoted by tenascin and inhibited by thrombospondin-1.
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Kaplony, A., D. R. Zimmermann, R. W. Fischer, et al. "Tenascin Mr 220,000 isoform expression correlates with corneal cell migration." Development 112, no. 2 (1991): 605–14. http://dx.doi.org/10.1242/dev.112.2.605.
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The three isoforms of chicken tenascin, an extracellular matrix glycoprotein, are generated by alternatively spliced fibronectin type III domains. The resulting proteins migrate as bands of Mr 220,000 (ten220), Mr 200,000 (ten200) and Mr 190,000 (ten190) on SDS-PAGE. We describe here two monoclonal antibodies, one specific for ten220 (mAb T17) and another that recognizes all isoforms (mAb T16). These were used to examine the differential expression of isoforms during development. Most impressive is the close correlation between ten220 expression and cell migration in the embryonic cornea. Initially (stage 18), ten190/200 can be detected within the corneal epithelium and along the basement membranes of the lens and sclera. Ten220 appears within the primary stroma immediately prior to the invasion by neural-crest-derived cells. This expression is maintained during the subsequent migration of fibroblasts from the conjunctiva into the primary stroma. With the completion of migration and the marked increase in matrix synthesis by corneal fibroblasts, ten220 disappears. Ten190/200 remains in the region adjoining the endothelium, the Bowman's membrane and the adjacent stroma. The cell-migration-associated isoform is isolated from extracts of embryonic tissues as a homohexamer. Low molecular weight forms appeared absent but a new tenascin band of Mr 210,000 could be detected in brain extracts which may be a new isoform. We conclude that the synthesis of tenascin isoforms is under tight developmental control and speculate that a function of the additional domains is to facilitate cell migration.
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Chiquet, Matthias, Manuel Koch, Mark Matthisson, Michael Tannheimer, and Ruth Chiquet-Ehrismann. "Regulation of extracellular matrix synthesis by mechanical stress." Biochemistry and Cell Biology 74, no. 6 (1996): 737–44. http://dx.doi.org/10.1139/o96-080.
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The extracellular matrix (ECM) provides mechanical support to tissues and is a substrate for cell adhesion and differentiation. Cells bind to ECM via specific cell surface receptors such as integrins. When engaging with ECM ligands, these receptors can activate signal tranduction pathways within the cells and may act as mechanochemical transducers. Thus, interaction of cells with ECM can modulate gene expression although the exact mechanisms are not known. Among the genes that are, in part, controlled by cell–ECM interactions are those for certain ECM components themselves. Bone cells, for example, remodel their matrix and reorient bone trabeculae in response to mechanical strain. Recently, we found that fibroblasts attached to a strained collagen matrix produce more of the ECM glycoproteins tenascin and collagen XII than cells in a relaxed matrix. In vivo, these two proteins are specifically expressed in places where mechanical strain is high. We also showed that the chick tenascin gene promoter contains a novel cis-acting, "strain-responsive" element that causes enhanced transcription in cells attached to a strained collagen matrix. Similar enhancer elements might be present in the promoters of other genes induced by mechanical stress. It can be speculated that connective tissue cells sense force vectors in their ECM environment and react to altered mechanical needs by regulating the transcription of specific ECM genes; tins process is a prerequisite for matrix remodeling.Key words: extracellular matrix proteins, integrins, mechanical stress, gene regulation.
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Makhluf, Huda A., Joanna Stepniakowska, Stanley Hoffman, Edwin Smith, E. Carwile LeRoy, and Maria Trojanowska. "IL-4 Upregulates Tenascin Synthesis in Scleroderma and Healthy Skin Fibroblasts." Journal of Investigative Dermatology 107, no. 6 (1996): 856–59. http://dx.doi.org/10.1111/1523-1747.ep12331160.
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Yoon, Jeong Yong, Seung Yeon Lee, Sue Shin, Kang Sup Yoon, and Chris Hyunchul Jo. "Comparative Analysis of Platelet-rich Plasma Effect on Tenocytes from Normal Human Rotator Cuff Tendon and Human Rotator Cuff Tendon with Degenerative Tears." Clinics in Shoulder and Elbow 21, no. 1 (2018): 3–14. http://dx.doi.org/10.5397/cise.2018.21.1.3.
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BACKGROUND: Platelet-rich plasma (PRP) stimulates cell proliferation and enhances matrix gene expression and synthesis. However, there have been no comparative study of the PRP effect on the normal and degenerative tenocytes. The purpose of this study was to compare the effect of PRP on tenocytes from normal and degenerative tendon.METHODS: Tendon tissues were obtained from patients undergoing arthroscopic repair (n=9) and from healthy donors (n=3). Tenocytes were cultured with 10% (vol/vol) platelet-poor plasma, PRP activated with calcium, and PRP activated with calcium and thrombin. The total cell number was assessed at days 7 and 14. The expressions of type I and III collagen, decorin, tenascin-C, and scleraxis were evaluated by quantitative real-time reverse transcriptase polymerase chain reaction. The total collagen and glycosaminoglycan (GAG) synthesis was evaluated at days 7 and 14.RESULTS: No differences were observed between the groups at day 7, but cell proliferation was remarkably increased in tenocytes from the degenerative tendon at day 14. In both tenocyte groups, the gene expressions of type I and III collagen were up-regulated. GAG synthesis was greater in the normal tendon, whereas the expressions of decorin and tenascin-C were increased in tenocytes from the degenerative tendon. Tenocytes from the degenerative tendon had higher fold-change of GAG synthesis and a lower collagen III/I ratio than normal tenocytes.CONCLUSIONS: PRP promoted the cell proliferation and enhanced the synthesis of tendon matrix in both groups. PRP has a greater positive effect on cell proliferation, matrix gene expression and synthesis in tenocytes from degenerative tendon.
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Lipke, D. L., S. M. Aziz, J. A. Fagerland, M. Majesky, and S. S. Arcot. "Tenascin synthesis, deposition, and isoforms in monocrotaline-induced pulmonary hypertensive rat lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 2 (1996): L208—L215. http://dx.doi.org/10.1152/ajplung.1996.271.2.l208.
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Monocrotaline (MCT)-induced pulmonary hypertension is characterized by alterations in vascular extracellular matrix and neomuscularization of small blood vessels. Tenascin (TN) is a matrix glycoprotein which modulates cellular attachment, proliferation, and migration. The present study used immunohistochemistry and Northern analyses to examine the hypothesis that treatment of rats with the potent pneumotoxin MCT induces temporal alterations in TN synthesis/deposition in the affected lungs. MCT produced progressive pathological alterations in the cardiopulmonary system, including increased dry lung weight, right ventricular hypertrophy, and pulmonary hypertension by days 7, 14, and 21, respectively. TN positive foci were first observed in the parenchyma surrounding small muscularized pulmonary arteries in MCT-treated rats at day 4; these foci became both more pronounced and frequent as the disease progressed. TN was also observed in the media of the intrapulmonary artery at day 21. Northern analysis demonstrated increases in TN transcripts in MCT-treated rats as early as day 1. Furthermore, a unique transcript, apparently lacking some fibronectin type III-like units, was observed in mRNA extracted from these rats. These data demonstrate alterations in TN synthetic capacity and focal increases in TN deposition in lungs from MCT-treated rats and suggest that TN may be associated with the pathogenesis of pulmonary hypertension.
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Götz, Magdalena, Jürgen Bolz, Angret Joester, and Andreas Faissner. "Tenascin-C Synthesis and Influence on Axonal Growth During Rat Cortical Development." European Journal of Neuroscience 9, no. 3 (1997): 496–506. http://dx.doi.org/10.1111/j.1460-9568.1997.tb01627.x.
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Song, Fanglong, Dawei Jiang, Tianchen Wang, et al. "Mechanical Loading Improves Tendon-Bone Healing in a Rabbit Anterior Cruciate Ligament Reconstruction Model by Promoting Proliferation and Matrix Formation of Mesenchymal Stem Cells and Tendon Cells." Cellular Physiology and Biochemistry 41, no. 3 (2017): 875–89. http://dx.doi.org/10.1159/000460005.
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Background/Aims: This study investigated the effect of mechanical stress on tendon-bone healing in a rabbit anterior cruciate ligament (ACL) reconstruction model as well as cell proliferation and matrix formation in co-culture of bone-marrow mesenchymal stem cells (BMSCs) and tendon cells (TCs). Methods: The effect of continuous passive motion (CPM) therapy on tendon-bone healing in a rabbit ACL reconstruction model was evaluated by histological analysis, biomechanical testing and gene expressions at the tendon-bone interface. Furthermore, the effect of mechanical stretch on cell proliferation and matrix synthesis in BMSC/TC co-culture was also examined. Results: Postoperative CPM therapy significantly enhanced tendon-bone healing, as evidenced by increased amount of fibrocartilage, elevated ultimate load to failure levels, and up-regulated gene expressions of Collagen I, alkaline phosphatase, osteopontin, Tenascin C and tenomodulin at the tendon-bone junction. In addition, BMSC/TC co-culture treated with mechanical stretch showed a higher rate of cell proliferation and enhanced expressions of Collagen I, Collagen III, alkaline phosphatase, osteopontin, Tenascin C and tenomodulin than that of controls. Conclusion: These results demonstrated that proliferation and differentiation of local precursor cells could be enhanced by mechanical stimulation, which results in enhanced regenerative potential of BMSCs and TCs in tendon-bone healing.
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Lenz, O., L. J. Striker, T. A. Jacot, S. J. Elliot, P. D. Killen, and G. E. Striker. "Glomerular endothelial cells synthesize collagens but little gelatinase A and B." Journal of the American Society of Nephrology 9, no. 11 (1998): 2040–47. http://dx.doi.org/10.1681/asn.v9112040.
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Mesangial sclerosis is a major feature of progressive renal disease. The mesangium contains mesangial cells and is bounded by the peripheral glomerular basement membrane and endothelial cells. Mesangial cells synthesize and degrade extracellular matrix. Whereas both mesangial and endothelial cells synthesize extracellular matrix components, the degradative pathway, well studied in the former, has not been investigated in endothelial cells. This study examines lines of all three glomerular cell types derived from female B6SJLF1/J mice, as well as mRNA levels for collagens alpha1(I), alpha1(IV), alpha3 (IV), alpha5 (IV), and alpha1 (VI), laminin, tenascin, matrix metalloproteinase-2 (MMP-2), and MMP-9. Type I and IV collagen synthesis was confirmed by enzyme-linked immunosorbent assay. MMP-2 and MMP-9 enzyme activity was measured by zymography. It was found that glomerular endothelial cells are a significant source of collagens, laminin, and tenascin. However, they express only low levels of MMP-2 and no detectable MMP-9. Stimulation with exogenous transforming growth factor-beta1 leads to a significant increase in collagen I, tissue inhibitors of metalloproteinase-1, and MMP-9 in conditioned media. These data suggest that glomerular endothelial cells may play an active role in extracellular matrix remodeling in glomerular disease.
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Knittel, Thomas, Margarete Odenthal, Detlef Schuppan, et al. "Synthesis of undulin by rat liver fat-storing cells: Comparison with fibronectin and tenascin." Experimental Cell Research 203, no. 2 (1992): 312–20. http://dx.doi.org/10.1016/0014-4827(92)90004-r.
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Evrova, Olivera, Damian Kellenberger, Maurizio Calcagni, Viola Vogel, and Johanna Buschmann. "Supporting Cell-Based Tendon Therapy: Effect of PDGF-BB and Ascorbic Acid on Rabbit Achilles Tenocytes In Vitro." International Journal of Molecular Sciences 21, no. 2 (2020): 458. http://dx.doi.org/10.3390/ijms21020458.
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Cell-based tendon therapies with tenocytes as a cell source need effective tenocyte in vitro expansion before application for tendinopathies and tendon injuries. Supplementation of tenocyte culture with biomolecules that can boost proliferation and matrix synthesis is one viable option for supporting cell expansion. In this in vitro study, the impacts of ascorbic acid or PDGF-BB supplementation on rabbit Achilles tenocyte culture were studied. Namely, cell proliferation, changes in gene expression of several ECM and tendon markers (collagen I, collagen III, fibronectin, aggrecan, biglycan, decorin, ki67, tenascin-C, tenomodulin, Mohawk, α-SMA, MMP-2, MMP-9, TIMP1, and TIMP2) and ECM deposition (collagen I and fibronectin) were assessed. Ascorbic acid and PDGF-BB enhanced tenocyte proliferation, while ascorbic acid significantly accelerated the deposition of collagen I. Both biomolecules led to different changes in the gene expression profile of the cultured tenocytes, where upregulation of collagen I, Mohawk, decorin, MMP-2, and TIMP-2 was observed with ascorbic acid, while these markers were downregulated by PDGF-BB supplementation. Vice versa, there was an upregulation of fibronectin, biglycan and tenascin-C by PDGF-BB supplementation, while ascorbic acid led to a downregulation of these markers. However, both biomolecules are promising candidates for improving and accelerating the in vitro expansion of tenocytes, which is vital for various tendon tissue engineering approaches or cell-based tendon therapy.
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Zhao, Yun, Stephen L. Young, and J. Clarke McIntosh. "Induction of tenascin in rat lungs undergoing bleomycin-induced pulmonary fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 6 (1998): L1049—L1057. http://dx.doi.org/10.1152/ajplung.1998.274.6.l1049.
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Lung injury induced by bleomycin is associated with early inflammation and subsequent excessive deposition of extracellular matrix. In the present study, we investigated the expression of extracellular matrix glycoprotein tenascin (TN) during pulmonary injury induced by bleomycin. After the initial lung injury induced by intratracheal bleomycin instillation, TN and collagen type III (COL III) mRNAs were greatly induced. The pattern of induction of TN was distinct from that of COL III. TN was primarily induced during the early inflammatory phase, whereas the increase in COL III synthesis continued during the reparative phase. The induction and localization of TN mRNA during bleomycin-induced pulmonary injury were also examined by in situ hybridization. TN mRNA was focally induced in rat lungs 3 days after bleomycin administration. Induction of TN mRNA was spatially restricted in the areas of tissue inflammation. The interstitial cells in alveolar septal walls and secondary septal tips in the areas of tissue damage were the major source of TN mRNA production. Expression of TN mRNA was decreased as the inflammation attenuated and development of fibrosis proceeded. Immunocytochemical analyses of TN protein distribution in the lung yielded corroborative results. Immunoreactive TN protein was found in a patchy distribution in alveolar septal walls and secondary septal tips in the areas of damaged tissues. This study demonstrated that TN is a unique early-response extracellular matrix component to bleomycin-induced pulmonary injury and is induced at the sites of the inflammation, suggesting a potential role of TN as a modulator of pulmonary inflammation and repair.
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Flück, Martin, Silvia Schmutz, Matthias Wittwer, Hans Hoppeler, and Dominique Desplanches. "Transcriptional reprogramming during reloading of atrophied rat soleus muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 1 (2005): R4—R14. http://dx.doi.org/10.1152/ajpregu.00833.2004.
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The hypothesis was tested that differential, coregulated transcriptional adaptations of various cellular pathways would occur early with increased mechanical loading of atrophied skeletal muscle and relate to concurrent damage of muscle fibers. Atrophy and slow-to-fast fiber transformation of rat soleus muscle was provoked by 14 days of hindlimb suspension (HS). Subsequent reloading of hindlimbs caused a fourfold increase in the percentage of muscle fibers, demonstrating endomysial tenascin-C staining. Five days after reloading, when 10% of the fibers were damaged, the normal muscle weight and slow-type fiber percentage were reestablished. Microarray analysis revealed major, biphasic patterns of gene expressional alterations with reloading that distinguish between treatments and gene ontologies. Transcript levels of factors involved in protein synthesis and certain proteasomal mRNAs were increased after 1 day of reloading and correlated to the percentage of fibers surrounded by tenascin-C. By contrast, levels of gene messages for fatty acid transporters, respiratory chain constituents, and voltage-gated cation channels were transiently reduced after 1 day of muscle loading and associated with the number of damaged fibers and the regain in muscle weight. This coregulation points toward important retooling of oxidative metabolism and the T- and SR-tubular systems with rebuilding of slow fibers. The observations demonstrate that early nuclear reprogramming with reloading of atrophic soleus muscle is coordinated and links to the processes involved in mechanical damage and regeneration of muscle fibers.
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Kau, S., I. Miller, A. Tichy, and C. Gabriel. "S100A4 (metastasin) positive mesenchymal canine mammary tumour spheroids reduce Tenascin C synthesis under DMSO exposurein vitro." Veterinary and Comparative Oncology 15, no. 4 (2017): 1428–44. http://dx.doi.org/10.1111/vco.12287.
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Hindermann, Winfried, Alexander Berndt, Laura Borsi, et al. "Synthesis and protein distribution of the unspliced large tenascin-C isoform in oral squamous cell carcinoma." Journal of Pathology 189, no. 4 (1999): 475–80. http://dx.doi.org/10.1002/(sici)1096-9896(199912)189:4<475::aid-path462>3.0.co;2-v.
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Ruhmann, Michaela, Anna M. Piccinini, Philip L. Kong, and Kim S. Midwood. "Endogenous activation of adaptive immunity: Tenascin-C drives interleukin-17 synthesis in murine arthritic joint disease." Arthritis & Rheumatism 64, no. 7 (2012): 2179–90. http://dx.doi.org/10.1002/art.34401.
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Koch, Manuel, Bernhard Wehrle-Haller, Stefan Baumgartner, Jürg Spring, Dorothee Brubacher, and Matthias Chiquet. "Epithelial synthesis of tenascin at tips of growing bronchi and graded accumulation in basement membrane and mesenchyme." Experimental Cell Research 194, no. 2 (1991): 297–300. http://dx.doi.org/10.1016/0014-4827(91)90368-5.
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Giannini, Giuseppe, Ferdinando Maria Milazzo, Gianfranco Battistuzzi, et al. "Synthesis and preliminary in vitro evaluation of DOTA-Tenatumomab conjugates for theranostic applications in tenascin expressing tumors." Bioorganic & Medicinal Chemistry 27, no. 15 (2019): 3248–53. http://dx.doi.org/10.1016/j.bmc.2019.05.047.
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Galtrey, Clare M., Jessica C. F. Kwok, Daniela Carulli, Kate E. Rhodes, and James W. Fawcett. "Distribution and synthesis of extracellular matrix proteoglycans, hyaluronan, link proteins and tenascin-R in the rat spinal cord." European Journal of Neuroscience 27, no. 6 (2008): 1373–90. http://dx.doi.org/10.1111/j.1460-9568.2008.06108.x.
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Kim, Won, Seul Ki Lee, Young-Won Kwon, Sun G. Chung, and and Soo Kim. "Pioglitazone-Primed Mesenchymal Stem Cells Stimulate Cell Proliferation, Collagen Synthesis and Matrix Gene Expression in Tenocytes." International Journal of Molecular Sciences 20, no. 3 (2019): 472. http://dx.doi.org/10.3390/ijms20030472.
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Various therapeutic effects of mesenchymal stem cells (MSCs) have been reported. However, the rapid clearance of these cells in vivo, difficulties in identifying their therapeutic mechanism of action, and insufficient production levels remain to be resolved. We investigated whether a pioglitazone pre-treatment of MSCs (Pio-MSCs) would stimulate the proliferation of co-cultured tenocytes. Pioglitazone increased the proliferation of MSCs and enhanced the secretion of VEGF (vascular endothelial growth factor) and collagen in these cells. We then examined the effects of Pio-MSCs on tenocytes using an indirect transwell culture system. A significant increase in tenocyte proliferation and cell cycle progression was observed in these co-cultures. Significant increases were observed in wound scratch closure by tenocytes from a Pio-MSC co-culture. Pio-MSCs also enhanced the secretion of collagen from tenocytes. A higher mRNA level of collagen type 1 (Col 1) and type 3 (Col 3), scleraxis (Scx), and tenascin C (TnC) was found in the tenocytes in Pio-MSC co-cultures compared with monocultured cells or tenocytes cultured with non-treated MSCs. Our results indicate that pioglitazone enhances the therapeutic effects of MSCs on tendon repair.
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Pattabiraman, Padmanabhan P., and Ponugoti Vasantha Rao. "Mechanistic basis of Rho GTPase-induced extracellular matrix synthesis in trabecular meshwork cells." American Journal of Physiology-Cell Physiology 298, no. 3 (2010): C749—C763. http://dx.doi.org/10.1152/ajpcell.00317.2009.
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Elevated intraocular pressure arising from impaired aqueous humor drainage through the trabecular pathway is a major risk factor for glaucoma. To understand the molecular basis for Rho GTPase-mediated resistance to aqueous humor drainage, we investigated the possible interrelationship between actomyosin contractile properties and extracellular matrix (ECM) synthesis in human trabecular meshwork (TM) cells expressing a constitutively active form of RhoA (RhoAV14). TM cells expressing RhoAV14 exhibited significant increases in fibronectin, tenascin C, laminin, α-smooth muscle actin (α-SMA) levels, and matrix assembly in association with increased actin stress fibers and myosin light-chain phosphorylation. RhoAV14-induced changes in ECM synthesis and actin cytoskeletal reorganization were mimicked by lysophosphatidic acid and TGF-β2, known to increase resistance to aqueous humor outflow and activate Rho/Rho kinase signaling. RhoAV14, lysophosphatidic acid, and TGF-β2 stimulated significant increases in Erk1/2 phosphorylation, paralleled by profound increases in fibronectin, serum response factor (SRF), and α-SMA expression. Treatment of RhoA-activated TM cells with inhibitors of Rho kinase or Erk, on the other hand, decreased fibronectin and α-SMA levels. Although suppression of SRF expression (both endogenous and RhoA, TGF-β2-stimulated) via the use of short hairpin RNA decreased α-SMA levels, fibronectin was unaffected. Conversely, fibronectin induced α-SMA expression in an SRF-dependent manner. Collectively, data on RhoA-induced changes in actomyosin contractile activity, ECM synthesis/assembly, and Erk activation, along with fibronectin-induced α-SMA expression in TM cells, reveal a potential molecular interplay between actomyosin cytoskeletal tension and ECM synthesis/assembly. This interaction could be significant for the homeostasis of aqueous humor drainage through the pressure-sensitive trabecular pathway.
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Rettig, W. J., H. P. Erickson, A. P. Albino, and P. Garin-Chesa. "Induction of human tenascin (neuronectin) by growth factors and cytokines: cell type-specific signals and signalling pathways." Journal of Cell Science 107, no. 2 (1994): 487–97. http://dx.doi.org/10.1242/jcs.107.2.487.
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The extracellular matrix protein tenascin (TN) is expressed with precise temporo-spatial patterns during embryonic and fetal development and is induced in healing wounds, inflammatory lesions and solid tumors. These tissue patterns suggest that TN synthesis may be modulated by soluble factors present in developing tissues or released from injured, inflammatory or neoplastic cells. To characterize the extrinsic control of human TN we examined the effects of several signalling molecules on cultured neural, melanocytic and fibroblastic cells. Results obtained with alpha TN antibodies in enzyme-linked immunosorbent and immunoprecipitation assays indicate that TN expression is tightly regulated in a cell type-specific manner: (1) Primitive neuroectodermal tumor (PNET) cells grown in chemically defined, serum-free media show up to &gt; 100-fold TN induction in response to fibroblast growth factors (aFGF, bFGF, K-FGF) and phorbol ester, independent of changes in cell proliferation or total protein synthesis; no induction is seen in PNET cultures stimulated with serum or other growth and differentiation factors. (2) Normal melanocytes, which require FGF and phorbol ester for survival in vitro, fail to express TN; however, they produce TN following oncogenic transformation. (3) Fibroblasts derived from disparate tissues differ up to 100-fold in basal TN production; for example, fetal lung fibroblasts are TNhigh, but conjunctival fibroblasts derived from the same donors and fetal leptomeningeal cells are TNlow. (4) TNlow fibroblasts treated with interleukin-1, tumor necrosis factor-alpha, and interleukin-4 show up to &gt; 100-fold increased TN secretion and TN incorporation into their extracellular matrix. Transforming growth factor-beta, which acts as an inducer of fibronectin, collagen, and integrin-type matrix receptors, has variable effects on fibroblast TN, ranging from increased deposition in the extracellular matrix of fetal conjunctival fibroblasts to reduced secretion in newborn foreskin fibroblasts. In contrast, FGFs (which are potent fibroblast mitogens), phorbol ester, bone morphogenetic proteins, and several other factors tested produced no discernible effects on fibroblast TN expression. These findings suggest that discrete sets of extrinsic signals modify TN expression in specific cell types, with the effects of a given ligand/receptor system determined by cell type-specific signalling pathways that may be linked to unique cis-regulatory elements of the TN gene. As a result, a limited set of regulatory peptides may produce highly diversified TN distribution patterns in developing and lesional tissues.
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Chassagne, Catherine, Christophe Adamy, Philippe Ratajczak, et al. "Angiotensin II AT2 receptor inhibits smooth muscle cell migration via fibronectin cell production and binding." American Journal of Physiology-Cell Physiology 282, no. 4 (2002): C654—C664. http://dx.doi.org/10.1152/ajpcell.00318.2001.
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To explore the vascular function of the angiotensin II (ANG II) AT2receptor subtype (AT2R), we generated a vascular smooth muscle cell (SMC) line expressing the AT2R (SMC-vAT2). The involvement of AT2R in the motility response of SMCs was examined in SMC-vAT2 cells and their controls (SMC-v) cultured on either laminin or fibronectin matrix proteins with the agarose drop technique. All experiments were conducted in the presence of a saturating concentration of losartan to inactivate the AT1R subtype. Under basal conditions, both cell lines migrated outside drops, but on laminin only. Treatment with ANG II significantly inhibited the migration of SMC-vAT2but not SMC-v cells, and this effect was prevented by the AT2R antagonist CGP-42112A. The decreased migration of SMC-vAT2 was not associated with changes in cell growth, cytoskeleton stiffness, or smooth muscle actin, desmin, and tenascin expression. However, it was correlated with increased synthesis and binding of fibronectin. Both responses were prevented by incubation with selective AT2R antagonists. Addition of GRGDTP peptide, which prevents cell attachment of fibronectin, reversed the AT2R inhibitory effect on SMC-vAT2 migration. These results suggest that activated ANG II AT2R inhibits SMC migration via cellular fibronectin synthesis and associated cell binding.
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Gore-Hyer, Elizabeth, Daniel Shegogue, Malgorzata Markiewicz та ін. "TGF-β and CTGF have overlapping and distinct fibrogenic effects on human renal cells". American Journal of Physiology-Renal Physiology 283, № 4 (2002): F707—F716. http://dx.doi.org/10.1152/ajprenal.00007.2002.
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Transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF) are ubiquitously expressed in various forms of tissue fibrosis, including fibrotic diseases of the kidney. To clarify the common and divergent roles of these growth factors in the cells responsible for pathological extracellular matrix (ECM) deposition in renal fibrosis, the effects of TGF-β and CTGF on ECM expression in primary human mesangial (HMCs) and human proximal tubule epithelial cells (HTECs) were studied. Both TGF-β and CTGF significantly induced collagen protein expression with similar potency in HMCs. Additionally, α2(I)-collagen promoter activity and mRNA levels were similarly induced by TGF-β and CTGF in HMCs. However, only TGF-β stimulated collagenous protein synthesis in HTECs. HTEC expression of tenascin-C (TN-C) was increased by TGF-β and CTGF, although TGF-β was the more potent inducer. Thus both growth factors elicit similar profibrogenic effects on ECM production in HMCs, while promoting divergent effects in HTECs. CTGF induction of TN-C, a marker of epithelial-mesenchymal transdifferentiation (EMT), with no significant induction of collagenous protein synthesis in HTECs, may suggest a more predominant role for CTGF in EMT rather than induction of excessive collagen deposition by HTECs during renal fibrosis.
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Kanta, Jiri, and Anna Zavadakova. "Role of fibronectin in chronic venous diseases: A review." Vascular Medicine 25, no. 6 (2020): 588–97. http://dx.doi.org/10.1177/1358863x20947789.
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Fibronectin (FN) circulating in the blood and produced by cells provides the basis of the extracellular matrix (ECM) formed in healing acute wounds. The time-dependent deposition of FN by macrophages, its synthesis by fibroblasts and myofibroblasts, and later degradation in the remodeled granulation tissue are a prerequisite for successful healing of wounds. However, the pattern of FN expression and deposition in skin lesions is disturbed. The degradation of the ECM components including FN in varicose veins prevails over ECM synthesis and deposition. FN is inconspicuous in the fibrotic lesions in lipodermatosclerosis, while tenascin-C containing FN-like peptide sequences are prominent. FN is produced in large amounts by fibroblasts at the edge of venous ulcers but FN deposition at the wound bed is impaired. Both the proteolytic environment in the wounds and the changed function of the ulcer fibroblasts may be responsible for the poor healing of venous ulcers. The aim of this review is to describe the current knowledge of FN pathophysiology in chronic venous diseases. In view of the fact that FN plays a crucial role in organizing the ECM, further research focused on FN metabolism in venous diseases may bring results applicable to the treatment of the diseases.
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Tremble, P., R. Chiquet-Ehrismann, and Z. Werb. "The extracellular matrix ligands fibronectin and tenascin collaborate in regulating collagenase gene expression in fibroblasts." Molecular Biology of the Cell 5, no. 4 (1994): 439–53. http://dx.doi.org/10.1091/mbc.5.4.439.
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Tenascin (TN) is a large oligomeric glycoprotein that is present transiently in the extracellular matrix (ECM) of cells and is involved in morphogenetic movements, tissue patterning, and tissue repair. It has multiple domains, both adhesive and anti-adhesive, that interact with cells and with fibronectin (FN) and other ECM macromolecules. We have studied the consequences of the interaction of TN with a FN matrix on gene expression in rabbit synovial fibroblasts. Fibroblasts plated on a mixed substrate of FN and TN, but not on FN alone, upregulated synthesis of four genes: collagenase, stromelysin, the 92-kDa gelatinase, and c-fos. Although the fibroblasts spread well on both FN and FN/TN substrates, nuclear c-Fos increased within 1 h only in cells that were plated on FN/TN. TN did not induce the expression of collagenase in cells plated on substrates of type I collagen or vitronectin (VN). Moreover, soluble TN added to cells adhering to a FN substrate or to serum proteins had no effect, suggesting that TN has an effect only in the context of mixed substrates of FN and TN. Collagenase increased within 4 h of plating on a FN/TN substrate and exhibited kinetics similar to those for induction of collagenase gene expression by signaling through the integrin FN receptor. Arg-Gly-Asp peptide ligands that recognize either the FN receptor or the VN receptor and function-perturbing anti-integrin monoclonal antibodies diminished the interaction of fibroblasts with a mixed substrate of FN, TN, and VN, but had no effect on the adhesion of fibroblasts to a substrate of FN and VN, suggesting that both receptors recognize the complex. Anti-TN68, an antibody that recognizes an epitope in the carboxyl-terminal type III repeats involved in the interaction of TN with both FN and cells, blocked the inductive effect of the FN/TN substrate, whereas anti-TNM1, an antibody that recognizes an epitope in the amino-terminal anti-adhesive region of epidermal growth factor-like repeats, had no effect. These data suggest that transient alteration of the composition of ECM by addition of proteins like TN may regulate the expression of genes involved in cell migration, tissue remodeling, and tissue invasion, in regions of tissue undergoing phenotypic changes.
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Fujinaga, Kazuya, Koji Onoda, Kiyohito Yamamoto, et al. "Locally applied cilostazol suppresses neointimal hyperplasia by inhibiting tenascin-C synthesis and smooth muscle cell proliferation in free artery grafts." Journal of Thoracic and Cardiovascular Surgery 128, no. 3 (2004): 357–63. http://dx.doi.org/10.1016/j.jtcvs.2003.11.015.
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Linnala, Auli, Veli-Pekka Lehto, and Ismo Virtanen. "Neuronal differentiation in SH-SY5Y human neuroblastoma cells induces synthesis and secretion of tenascin and upregulation of ?v integrin receptors." Journal of Neuroscience Research 49, no. 1 (1997): 53–63. http://dx.doi.org/10.1002/(sici)1097-4547(19970701)49:1<53::aid-jnr6>3.0.co;2-c.
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Kirsch, Schreiber, Dienes, Böttger, and Junginger. "Veränderungen der extrazellulären Matrix in der varikösen Venenwand." Vasa 28, no. 2 (1999): 95–99. http://dx.doi.org/10.1024/0301-1526.28.2.95.
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Background: Investigation of changes in normal veins which result in the formation of varicosis led to examination of the histological organisation of the vessel wall and to histomorphological alterations in the region of the extracellular matrix. Patients and methods: The expression pattern of the matrix proteins collagen IV, fibronectin, laminin, tenascin, and undulin as well as the structure and orientation of elastic fibres were determined by means of immunohistochemical staining. Results: All varices exhibited an increased expression pattern in comparison to healthy veins. The venous vessel wall was often non-homogeneously enlarged. The intima was always more involved than the media and showed enhanced accumulation, whereas, the adventitia was not influenced by the pathological process. Collagen IV exhibited an early accumulation, especially in the subendothelial region. The other matrix proteins demonstrated an increase in fibre propagation parallel to the enlargement of the vessel wall. Essentially, an augmented de novo synthesis of fibres with an irregular arrangement and the formation of local plaques was found. Elastic fibres were enhanced by slight involvement of the vessel wall and were reduced and fragmented during increased involvement of the venous wall which explained the rigidity of varices in contrast to normal veins.
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Truong, L. D., M. W. Majesky, and J. Pindur. "Tenascin is synthesized and secreted by rat mesangial cells in culture and is present in extracellular matrix in human glomerular diseases." Journal of the American Society of Nephrology 4, no. 10 (1994): 1771–77. http://dx.doi.org/10.1681/asn.v4101771.
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Tenascin (TN) is a large oligomeric protein recently described as a component of the extracellular matrix. The distribution of TN in adult kidney tissue has not been adequately evaluated, but preliminary data have suggested that TN is variably seen in rare mesangial areas and in stroma surrounding some tubules. The enlargement of the mesangial matrix (mesangial sclerosis) is a common feature of many renal diseases and is thought to be partially related to oversynthesis of the normal components of the mesangial matrix (collagen type IV, laminin, fibronectin, and heparan sulfate proteoglycans) by mesangial cells. However, the possibility that mesangial cells are also the source of other extracellular matrix proteins that participate in the process of mesangial sclerosis has not been explored. In this study, the synthesis of TN by cultured rat mesangial cells was documented by the following observations: (1) Northern hybridization of total RNA extracted from mesangial cells showed two distinct species of TN mRNA; (2) immunoblotting of the protein extracted from the conditioned medium demonstrated four TN protein bands; (3) immunoblotting of the protein extracted from the mesangial cell lysate demonstrated at least four TN protein bands; and (4) immunohistochemical techniques identified TN within the cytoplasm of mesangial cells and in the surrounding extracellular matrix.(ABSTRACT TRUNCATED AT 250 WORDS)
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Haydont, Valérie, Véronique Neiveyans, Philippe Perez, et al. "Fibroblasts from the Human Skin Dermo-Hypodermal Junction are Distinct from Dermal Papillary and Reticular Fibroblasts and from Mesenchymal Stem Cells and Exhibit a Specific Molecular Profile Related to Extracellular Matrix Organization and Modeling." Cells 9, no. 2 (2020): 368. http://dx.doi.org/10.3390/cells9020368.
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Human skin dermis contains fibroblast subpopulations in which characterization is crucial due to their roles in extracellular matrix (ECM) biology. This study investigates the properties of fibroblasts localized at the frontier of deep dermis and hypodermis, i.e., dermo-hypodermal junction fibroblasts (F-DHJ), which were compared to intermediate reticular dermis (Fr) and superficial papillary dermis (Fp) fibroblasts. F-DHJ differed from Fr and Fp cells in their wider potential for differentiation into mesodermal lineages and in their absence of contractility when integrated in a three-dimensional dermal equivalent. The transcriptomic profile of F-DHJ exhibited specificities in the expression of genes involved in ECM synthesis-processing and “tissue skeleton” organization. In accordance with transcriptome data, ECM proteins, notably Tenascin C, distributions differed between the reticular dermis and the dermo-hypodermal junction areas, which was documented in normal adult skin. Finally, genome-wide transcriptome profiling was used to evaluate the molecular proximity of F-DHJ with the two dermal fibroblast populations (Fp and Fr) and with the mesenchymal stem cells (MSCs) corresponding to five tissue origins (bone marrow, fat, amnion, chorion, and cord). This comparative analysis classified the three skin fibroblast types, including F-DHJ, as a clearly distinct group from the five MSC sample origins.
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Liu, Xing, Adrien Baldit, Emilie de Brosses, et al. "Characterization of Bone Marrow and Wharton’s Jelly Mesenchymal Stromal Cells Response on Multilayer Braided Silk and Silk/PLCL Scaffolds for Ligament Tissue Engineering." Polymers 12, no. 9 (2020): 2163. http://dx.doi.org/10.3390/polym12092163.
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(1) Background: A suitable scaffold with adapted mechanical and biological properties for ligament tissue engineering is still missing. (2) Methods: Different scaffold configurations were characterized in terms of morphology and a mechanical response, and their interactions with two types of stem cells (Wharton’s jelly mesenchymal stromal cells (WJ-MSCs) and bone marrow mesenchymal stromal cells (BM-MSCs)) were assessed. The scaffold configurations consisted of multilayer braids with various number of silk layers (n = 1, 2, 3), and a novel composite scaffold made of a layer of copoly(lactic acid-co-(e-caprolactone)) (PLCL) embedded between two layers of silk. (3) Results: The insertion of a PLCL layer resulted in a higher porosity and better mechanical behavior compared with pure silk scaffold. The metabolic activities of both WJ-MSCs and BM-MSCs increased from day 1 to day 7 except for the three-layer silk scaffold (S3), probably due to its lower porosity. Collagen I (Col I), collagen III (Col III) and tenascin-c (TNC) were expressed by both MSCs on all scaffolds, and expression of Col I was higher than Col III and TNC. (4) Conclusions: the silk/PLCL composite scaffolds constituted the most suitable tested configuration to support MSCs migration, proliferation and tissue synthesis towards ligament tissue engineering.
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Burk, Janina, Amelie Plenge, Walter Brehm, Sandra Heller, Bastian Pfeiffer, and Cornelia Kasper. "Induction of Tenogenic Differentiation Mediated by Extracellular Tendon Matrix and Short-Term Cyclic Stretching." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/7342379.
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Tendon and ligament pathologies are still a therapeutic challenge, due to the difficulty in restoring the complex extracellular matrix architecture and biomechanical strength. While progress is being made in cell-based therapies and tissue engineering approaches, comprehensive understanding of the fate of progenitor cells in tendon healing is still lacking. The aim of this study was to investigate the effect of decellularized tendon matrix and moderate cyclic stretching as natural stimuli which could potentially direct tenogenic fate. Equine adipose-derived mesenchymal stromal cells (MSC) were seeded on decellularized tendon matrix scaffolds. Mechanical stimulation was applied in a custom-made cyclic strain bioreactor. Assessment was performed 4 h, 8 h, and 24 h following mechanical stimulation. Scaffold culture induced cell alignment and changes in expression of tendon-related genes, although cell viability was decreased compared to monolayer culture. Short mechanical stimulation periods enhanced most of the scaffold-induced effects. Collagen 1A2 expression levels were decreased, while collagen 3A1 and decorin levels were increased. Tenascin-C and scleraxis expression showed an initial decrease but had increased 24 h after stimulation. The results obtained suggest that decellularized tendon matrix, supported by cyclic stretching, can induce tenogenic differentiation and the synthesis of tendon components important for matrix remodeling.
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Pfander, D. "Tenascin and aggrecan expression by articular chondrocytes is influenced by interleukin 1 : a possible explanation for the changes in matrix synthesis during osteoarthritis." Annals of the Rheumatic Diseases 63, no. 3 (2004): 240–44. http://dx.doi.org/10.1136/ard.2002.003749.
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Gögele, Clemens, Judith Hahn, Cindy Elschner та ін. "Enhanced Growth of Lapine Anterior Cruciate Ligament-Derived Fibroblasts on Scaffolds Embroidered from Poly(l-lactide-co-ε-caprolactone) and Polylactic Acid Threads Functionalized by Fluorination and Hexamethylene Diisocyanate Cross-Linked Collagen Foams". International Journal of Molecular Sciences 21, № 3 (2020): 1132. http://dx.doi.org/10.3390/ijms21031132.
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Reconstruction of ruptured anterior cruciate ligaments (ACLs) is limited by the availability and donor site morbidity of autografts. Hence, a tissue engineered graft could present an alternative in the future. This study was undertaken to determine the performance of lapine (L) ACL-derived fibroblasts on embroidered poly(l-lactide-co-ε-caprolactone) (P(LA-CL)) and polylactic acid (PLA) scaffolds in regard to a tissue engineering approach for ACL reconstruction. Surface modifications of P(LA-CL)/PLA by gas-phase fluorination and cross-linking of a collagen foam using either ethylcarbodiimide (EDC) or hexamethylene diisocyanate (HMDI) were tested regarding their influence on cell adhesion, growth and gene expression. The experiments were performed using embroidered P(LA-CL)/PLA scaffolds that were seeded dynamically or statically with LACL-derived fibroblasts. Scaffold cytocompatibility, cell survival, numbers, metabolic activity, ultrastructure and sulfated glycosaminoglycan (sGAG) synthesis were evaluated. Quantitative real-time polymerase chain reaction (QPCR) revealed gene expression of collagen type I (COL1A1), decorin (DCN), tenascin C (TNC), Mohawk (MKX) and tenomodulin (TNMD). All tested scaffolds were highly cytocompatible. A significantly higher cellularity and larger scaffold surface areas colonized by cells were detected in HMDI cross-linked and fluorinated scaffolds compared to those cross-linked with EDC or without any functionalization. By contrast, sGAG synthesis was higher in controls. Despite the fact that the significance level was not reached, gene expressions of ligament extracellular matrix components and differentiation markers were generally higher in fluorinated scaffolds with cross-linked collagen foams. LACL-derived fibroblasts maintained their differentiated phenotype on fluorinated scaffolds supplemented with a HMDI cross-linked collagen foam, making them a promising tool for ACL tissue engineering.
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Sharma, K., and F. N. Ziyadeh. "The emerging role of transforming growth factor-beta in kidney diseases." American Journal of Physiology-Renal Physiology 266, no. 6 (1994): F829—F842. http://dx.doi.org/10.1152/ajprenal.1994.266.6.f829.
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Transforming growth factor-beta (TGF-beta) is a prototypical multifunctional cytokine, with growth being only one of its many functions. Its receptors and actions are germane to almost every cell in the body involved in tissue injury and repair, and its effects are best understood in the context of a cellular response to a changing environment. The broad areas in which TGF-beta plays a crucial role include cell proliferation and extracellular matrix production. TGF-beta is a key regulatory molecule in the control of the activity of fibroblasts and has been implicated in several disease states characterized by excessive fibrosis. In the kidney, TGF-beta promotes tubuloepithelial cell hypertrophy and regulates the glomerular production of almost every known molecule of the extracellular matrix, including collagens, fibronectin, tenascin, and proteoglycans, as well as the integrins that are the receptors for these molecules. Furthermore, TGF-beta blocks the destruction of newly synthesized extracellular matrix by upregulating the synthesis of protease inhibitors and downregulating the synthesis of matrix-degrading proteases such as stromelysin and collagenase. As will be discussed, there is a strong body of in vitro and in vivo evidence suggesting that persistent overproduction of TGF-beta 1 in glomeruli after the acute inflammatory stage of glomerulonephritis causes glomerulosclerosis. TGF-beta may also be important in a variety of other chronic renal disorders characterized by hypertrophy and sclerosis, such as diabetic nephropathy. In this review we will attempt to offer a basic understanding of the cellular and molecular biology of TGF-beta and its receptors, with special focus on the role of the TGF-beta system in the kidney during development, growth, and disease.
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Jarvinen, T. A. H. "Mechanical loading regulates the expression of tenascin-C in the myotendinous junction and tendon but does not induce de novo synthesis in the skeletal muscle." Journal of Cell Science 116, no. 5 (2003): 857–66. http://dx.doi.org/10.1242/jcs.00303.
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