Tenascins: regulation and putative functions during pathological stress

Chiquet‐Ehrismann, Ruth; Chiquet, Matthias

doi:10.1002/path.1415

Cited by 483 publications

(437 citation statements)

References 163 publications

(166 reference statements)

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“…(Ghert et al 2001) It has both adhesive and anti-adhesive effects and is involved in cell migration, ECM remodeling, development, tumorogenesis and wound healing. (Chiquet-Ehrismann et al 1988;Vainio et al 1989;Ghert et al 2001;Bornstein and Sage 2002;Chiquet-Ehrismann and Chiquet 2003;ChiquetEhrismann 2004) Some of these processes occur via tenascin C's association with fibronectin fibrils and effects on fibronectin-cell interactions. (Chung et al 1995;Ghert et al 2001) In addition to exhibiting changes in levels with various treatments that modify outflow facility (see later), tenascin C also undergoes a number of changes in mRNA splicing (Keller et al, manuscript in preparation).…”

Section: Matricellular Proteinsmentioning

confidence: 99%

Extracellular matrix in the trabecular meshwork

Acott

Kelley

2008

Experimental Eye Research

424

443

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The extracellular matrix (ECM) of the trabecular meshwork (TM) is thought to be important in regulating intraocular pressure (IOP) in both normal and glaucomatous eyes. IOP is regulated primarily by a fluid resistance to aqueous humor outflow. However, neither the exact site nor the identity of the normal resistance to aqueous humor outflow has been established. Whether the site and nature of the increased outflow resistance, which is associated with open-angle glaucoma, is the same or different from the normal resistance is also unclear.The ECMs of the TM beams, juxtacanalicular region (JCT) and Schlemm's canal (SC) inner wall are comprised of fibrillar and non-fibrillar collagens, elastin-containing microfibrils, matricellular and structural organizing proteins, glycosaminoglycans (GAGs) and proteoglycans. Both basement membranes and stromal ECM are present in the TM beams and JCT region. Cell adhesion proteins, cell surface ECM receptors and associated binding proteins are also present in the beams, JCT and SC inner wall region.The outflow pathway ECM is relatively dynamic, undergoing constant turnover and remodeling. Regulated changes in enzymes responsible for ECM degradation and biosynthetic replacement are observed. IOP homeostasis, triggered by pressure changes or mechanical stretching of the TM, appears to involve ECM turnover. Several cytokines, growth factors and drugs, which affect the outflow resistance, change ECM component expression, mRNA alternative splicing, cellular cytoskeletal organization or all of these. Changes in ECM associated with open-angle glaucoma have been identified.

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Section: Matricellular Proteinsmentioning

confidence: 99%

Extracellular matrix in the trabecular meshwork

Acott

Kelley

2008

Experimental Eye Research

424

443

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“…Tenascin-C is an ECM glycoprotein, highly expressed in most tumors and early stages of development, but much restricted in developed tissues. 69,70 Overexpression of tenascin-C has been correlated with tumorigenesis and angiogenesis through regulation of oncogenes, tumor suppressor genes, genome integrity genes, and evading of immune surveillance. 71 Tenascin-C may inactivate cell cycle checkpoint genes in tumor cell to facilitate neoplastic phenotype expansion.…”

Section: Tumor Ecm In Microenvironmentmentioning

confidence: 99%

Breast Tumor Microenvironment: Proteomics Highlights the Treatments Targeting Secretome

et al. 2008

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Tumor secreted substances (secretome), including extracellular matrix (ECM) components, act as mediators of tumor-host communication in the breast tumor microenvironment. Proteomic analysis has emphasized the value of the secretome as a source of prospective markers and drug targets for the treatment of breast cancers. Utilizing bioinformatics, our recent studies revealed global changes in protein expression after the activation of ECM-mediated signaling in breast cancer cells. A newly designed technique integrating a capillary ultrafiltration (CUF) probe with mass spectrometry was demonstrated to dynamically sample and identify in vivo and pure secretome from the tumor microenvironment. Such in vivo profiling of breast cancer secretomes may facilitate the development of novel drugs specifically targeting secretome.

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“…Tenascin-C not only interacts with other ECM molecules, such as perlecan and fibronectin, but also cellsurface receptors including integrins a2b1, avb3 and a9b1, annexin II, and syndecan (40). It is proposed that the inhibition of syndecan-4, Rho, and FAK in cell spreading and the fibronectin matrix assembly by tenascin-C are major mechanisms for cell detachment operating in solid tumors (41,42).…”

Section: Discussionmentioning

confidence: 99%