Tenascin‐C is a useful marker for disease activity in myocarditis

Imanaka‐Yoshida, Kyoko; Hiroe, Michiaki; Yasutomi, Yasuhiro; Toyozaki, Tetsuya; Tsuchiya, Takuro; Noda, Naomi; Maki, Toshiki; Nishikawa, Toshio; Sakakura, Teruyo; Yoshida, Toshimichi

doi:10.1002/path.1131

Cited by 118 publications

(118 citation statements)

References 26 publications

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“…With cardiac injury and inflammation, its levels increase and tenascin-C is also used as a marker to show the severity of viral myocarditis 31) . Tenascin-C is also detected in the marginal zone between the infarcted area and the intact area after myocardial infarction 14,32) and it is thought to be a useful marker to predict left ventricular remodeling and prognosis after acute myocardial infarction 33) .…”

Section: Discussionmentioning

confidence: 99%

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Çelik

Koçyiğit

Çalapkorur

et al. 2011

JAT

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Aim:Numerous studies have shown an increase in NT-pro BNP, troponin and D-dimer levels with right ventricular dysfunction on echocardiography in patients with acute pulmonary thromboembolism (PTE). We found no data about the relation between tenascin-C and acute PTE in the literature. The aim of this study was to evaluate tenascin-C levels in acute PTE and correlate them with NT-pro BNP, troponin and D-dimer. Method: Thirty-four patients who have massive or submassive PTE on spiral thorax CT (PTE group) and twenty healthy volunteers (non-PTE group) were evaluated. In all patients, right ventricular functions were obtained on transthoracic echocardiography and plasma tenascin-C, NT-pro BNP, troponin , and D-dimer levels were measured. Results: The left ventricular systolic diameter, left ventricular diastolic diameter and left ventricular ejection fraction were similar in the two groups. The right heart chamber sizes and main pulmonary artery diameter were significantly larger in the PTE group and systolic pulmonary artery pressures were also significantly higher in this group. Tenascin-C, NT-pro BNP, and D-dimer levels were also significantly higher in the PTE group than in the non-PTE group ( p 0.001). The troponin I levels did not differ between the two groups ( p 0.4). Tenascin-C was found to be highly correlated with sPAP and NT-pro BNP and correlated with D-dimer; however, troponin I was not correlated with tenascin-C. Conclusion: This study demonstrates that tenascin-C may be an indicator of acute PTE. J Atheroscler Thromb, 2011; 18:487-493.

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Section: Discussionmentioning

confidence: 99%

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Çelik

Koçyiğit

Çalapkorur

et al. 2011

JAT

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“…Other organs and tissues in which tenascin-C was reported to be upregulated in conjunction with inflammation include kidney (IgA nephropathy [75]), liver (primary sclerosing cholangitis [76]), heart (autoimmune myocarditis [77]), and arteries (atherosclerosis [78]). …”

Section: Role Of Tenascin-c In Inflammationmentioning

confidence: 99%

Tenascins: regulation and putative functions during pathological stress

Chiquet‐Ehrismann

Chiquet

2003

The Journal of Pathology

483

414

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In this review, we discuss the structure and function of the extracellular matrix protein family of tenascins with emphasis on their involvement in human pathologies. The article is divided into the following sections: Introduction: the tenascin family of extracellular matrix proteins; Structural roles: tenascin-X deficiency and Ehlers-Danlos syndrome; Tenascins as modulators of cell adhesion, migration, and growth; Role of tenascin-C in inflammation; Regulation of tenascins by mechanical stress: implications for wound healing and regeneration; Association of tenascin-C with cancer: antibodies as diagnostic and therapeutic tools; Conclusion and perspectives.

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“…The monoclonal antibody 4F10TT against the EGF-like repeats of Tn-C was as previously reported. 42 The membranes were then washed in the blocking buffer and successively treated with peroxidase-labeled goat anti-mouse IgG Fab' (1: 400, MBL, Nagoya, Japan) for 1 hour at room temperature. The reactive bands were developed with diaminobenzidine (DAB)/H 2 O 2 solution.…”

Section: Immunoblottingmentioning

confidence: 99%

Involvement of Large Tenascin-C Splice Variants in Breast Cancer Progression

Tsunoda

Inada

Kalembeyi

et al. 2003

The American Journal of Pathology

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104

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Alternative splicing of fibronectin-like type III (FNIII) repeats of tenascin-C (Tn-C) generates a number of splice variants. The distribution of large variants, typical components of provisional extracellular matrices that are up-regulated during tumor stroma remodeling, was here studied by immunoblotting and immunohistochemistry using a monoclonal antibody against the FNIII B domain (named 4C8MS) in a series of human breast cancers. Large Tn-C variants were found at only low levels in normal breast tissues, but were highly expressed at invading sites of intraductal cancers and in the stroma of invasive ductal cancers, especially at invasion fronts. There was a positive correlation between the expression of large Tn-C variants and the cell proliferation rate determined by immunolabeling of the Ki-67 antigen. Of the Tn-C recombinant fragments (all FNIII repeats or mFNIII FL, the conserved FNIII domain only, the epidermal growth factor-like domain, and the fibrinogen-like domain) which were expressed by CHO-K1 cells transfected with mouse Tn-C cDNAs, only the mFNIII FL enhanced in vitro migration and mitotic activity of mammary cancer cells derived from a Tn-C-null mouse. Addition of 4C8MS blocked the function of mFNIII FL. These findings provide strong evidence that the FNIII alternatively spliced region has important roles in tumor progression of breast cancer. During tumor progression, the cancer stroma becomes remodeled by both tumor cells and stromal cells, and protein components of the extracellular matrix (ECM) are dynamically changed by degradation and neosynthesis. Cellular interaction with the ECM strongly influences the behavior of cancer and stromal cells, resulting in modulation of cell growth, migration, differentiation, and apoptosis. 1-3 Compositional change of the ECM in cancer stroma is thus a key determinant of tumor growth and cancer progression. A variety of ECM glycoproteins, such as tenascin-C (Tn-C) and fibronectin, are overexpressed in cancer stroma. In addition, splice variants of these proteins, which are generally absent in normal adult tissues, become predominant. 4 -11 It has been reported that overexpression of Tn-C in breast cancer is related to a poor prognosis, and local and distant recurrence, 12-14 this being attributable to the ability to promote cell migration and proliferation demonstrated in vitro. 15,16 Tn-C is a hexameric glycoprotein, each subunit consisting of a TA (Tn assembly) domain; 14 ϩ 1/2 epidermal growth factor (EGF)-like domains, a variable number of fibronectin type III (FN III) repeats, and a C-terminal fibrinogen-related domain (FBG). [17][18][19][20][21] The size of Tn-C monomers varies as a result of alternative splicing in the FN III repeats at the pre-mRNA level. There are eight conserved FN III repeats (designated as numbers 1-8) and, in the case of human Tn-C, up to nine alternatively spliced FN III repeats (designated as letters A-D) inserted between the conserved repeats 5 and 6. In adults, the smallest Tn-C variant in which the alternatively splic...

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Tenascin‐C is a useful marker for disease activity in myocarditis

Cited by 118 publications

References 26 publications

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Tenascin-C May Be a Predictor of Acute Pulmonary Thromboembolism

Tenascins: regulation and putative functions during pathological stress

Involvement of Large Tenascin-C Splice Variants in Breast Cancer Progression

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