Interactions of human tenascin-X domains with dermal extracellular matrix molecules

Egging, David; Berkmortel, Franka van den; Taylor, Glen; Bristow, Jim; Schalkwijk, Joost

doi:10.1007/s00403-006-0706-9

Cited by 56 publications

(54 citation statements)

References 27 publications

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“…12) TNX haploinsufficiency is associated with joint hypermobility type of EDS. 14) Previous studies have indicated several functional properties of TNX, including collagen fibrillogenesis, 15,16) collagen deposition, 17) and development and maintenance of elastic fibers. 18) As for the adhesive properties of bovine TNX in which the 10th FNIII repeat possesses an Arg-Gly-Asp (RGD) putative cell attachment sequence, Elefteriou et al 9,19) demonstrated that osteosarcoma (MG63) and bladder carcinoma (ECV304) cells adhere to bovine TNX weakly and that do not spread and do not assemble actin stress fibers.…”

mentioning

confidence: 99%

Tenascin-X Induces Cell Detachment through p38 Mitogen-Activated Protein Kinase Activation

Fujie

Maita

Ariga

et al. 2009

Biological & Pharmaceutical Bulletin

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Extracellular matrix glycoprotein tenascin-X (TNX) is the largest member of the tenascin family. In this study, we investigated the adhesive properties of TNX and the signaling pathway to be induced to mouse fibroblast L cells on TNX substrate. Approximately 45% of evaluable cells used in the cell adhesion assay were attached to purified TNX but did not spread and were rounded on TNX. The remaining 55% of cells were detached from the TNX substrate and were floating in the conditioned medium. In rounded cells on TNX, phosphorylation of focal adhesion kinase (FAK) was diminished compared with that in cells on control phosphate buffered saline (PBS). To better understand the pathways that lead to the detachment of cells on the TNX substrate, we examined phosphorylation of p38 mitogen-activated protein (MAP) kinase. Phosphorylation of p38 MAP kinase was observed in the rounded cells on TNX in a dose-dependent manner, and the maximum effect was observed at 30 min on TNX. Inhibition of p38 MAP kinase a a expression by RNA interference partially suppressed the TNX-induced cell detachment. These results suggest that the p38 MAP kinase is a major mediator of TNX-induced cell detachment.

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confidence: 99%

Tenascin-X Induces Cell Detachment through p38 Mitogen-Activated Protein Kinase Activation

Fujie

Maita

Ariga

et al. 2009

Biological & Pharmaceutical Bulletin

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“…Moreover, these authors used a small isoform lacking the central FNIII modules, whereas we produced the full-length protein comprising 30 FNIII domains. Interestingly, another group has shown that the 29 th FNIII module of TNX accelerates collagen fibrillogenesis [8], but this modulatory effect seems to be masked in…”

Section: Influence Of Tnx On Collagen Fibrillogenesismentioning

confidence: 99%

“…Considering the interaction of TNX with fibrillar collagens [7,8] and the elastic properties of TNX [9], we decided to examine the physical behaviour of the collagen gels formed in the presence of TNX by rheometry, and to compare them to control gels consisting of collagen alone, or collagen and BSA.…”

Section: Effect Of Tnx On the Mechanical Properties Of Collagen Gelsmentioning

confidence: 99%

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Tenascin-X increases the stiffness of collagen gels without affecting fibrillogenesis

Margaron

Bostan

Exposito

et al. 2010

Biophysical Chemistry

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Tenascin-X is an extracellular matrix protein whose absence leads to an Ehlers-Danlos Syndrome in humans, mainly characterised by connective tissue defects including the disorganisation of fibrillar networks, a reduced collagen deposition, and modifications in the mechanical properties of dense tissues. Here we tested the effect of tenascin-X on in vitro collagen fibril formation. We observed that the main parameters of fibrillogenesis were unchanged, and that the diameter of fibrils was not significantly different when they were formed in the presence of tenascin-X. Interestingly, mechanical analysis of collagen gels showed an increased compressive resistance of the gels containing tenascin-X, indicating that this protein might be directly involved in determinating the mechanical properties of collagen-rich tissues in vivo.

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“…TNX-deficient mice partly mimic this phenotype. 3) Several observations suggest that TNX is involved in collagen fibrillogenesis, 4,5) collagen deposition, 6) modulation of collagen stiffness, 7) and development and maintenance of elastic fibers. 8) The serum form of TNX has also been identified in humans and mice.…”

mentioning

confidence: 99%

Increased Expression of Tenascin-X in Thoracic and Abdominal Aortic Aneurysm Tissues

Satoh

Tsukamoto

Shindoh

et al. 2010

Biological & Pharmaceutical Bulletin

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Tenascin-X (TNX), which has a molecular mass of roughly 450 kDa, is the largest member of the tenascin family. Complete deficiency of TNX in humans leads to a recessive form of Ehlers-Danlos syndrome (EDS). TNX is expressed abundantly in a variety of tissues, especially in cardiac muscle and in perivascular stroma. Human TNX is also present in serum with an apparent molecular size of 140 kDa. In the present study, we investigated the expression levels of TNX protein in thoracic and abdominal aortic aneurysm tissues. The level of TNX was significantly increased in both aortic aneurysm tissues compared with that in adjacent normal tissues. Next, to compare TNX levels in serum from both patients with thoracic aortic aneurysm and patients with abdominal aortic aneurysm with levels in serum from healthy individuals, we developed a sandwich enzyme-linked immunosorbent assay (ELISA) using TNX-specific antibodies. Measurement of TNX serum concentrations in both aortic aneurysm patients and controls showed that the levels were almost the same. These results indicate that TNX expression is significantly elevated in both thoracic and abdominal aortic aneurysm tissues but that the increase in TNX levels in both tissues does not result in an increase in TNX serum concentration in patients with TAA or AAA.

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Interactions of human tenascin-X domains with dermal extracellular matrix molecules

Cited by 56 publications

References 27 publications

Tenascin-X Induces Cell Detachment through p38 Mitogen-Activated Protein Kinase Activation

Tenascin-X Induces Cell Detachment through p38 Mitogen-Activated Protein Kinase Activation

Tenascin-X increases the stiffness of collagen gels without affecting fibrillogenesis

Increased Expression of Tenascin-X in Thoracic and Abdominal Aortic Aneurysm Tissues

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