Advances in tenascin-C biology

Midwood, Kim S.; Hussenet, Thomas; Langlois, Benoît; Orend, Gertraud

doi:10.1007/s00018-011-0783-6

Cited by 274 publications

(268 citation statements)

References 187 publications

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“…The antibody we used in the current study recognizes the EGF‐like domain and is suitable to measure total myocardial TNC level, because the subsequent fibronectin III domain contains a splice variant region that varies considerably in its expression form. The EGF‐like repeat domain interacts with the epidermal growth factor receptor, and the fibronectin III‐like repeat domain binds integrins to promote adhesion and mediates cell activation via toll‐like receptor 4, leading to sustained inflammation 23. The unfavourable effects of TNC on ventricular remodelling in DCM might result from ongoing myocardial damage or inability to repair the failing heart because of sustained inflammation.…”

Section: Discussionmentioning

confidence: 99%

Significance of myocardial tenascin‐C expression in left ventricular remodelling and long‐term outcome in patients with dilated cardiomyopathy

Yokokawa

Sugano

Nakayama

et al. 2016

European J of Heart Fail

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AimDilated cardiomyopathy (DCM) has a variety of causes, and no useful approach to predict left ventricular (LV) remodelling and long‐term outcome has yet been established. Myocardial tenascin‐C (TNC) is known to appear under pathological conditions, possibly to regulate cardiac remodelling. The aim of this study was to clarify the significance of myocardial TNC expression in LV remodelling and the long‐term outcome in DCM.Methods and resultsOne hundred and twenty‐three consecutive DCM patients who underwent endomyocardial biopsy for initial diagnosis were studied. Expression of TNC in biopsy sections was analysed immunohistochemically to quantify the ratio of the TNC‐positive area to the whole myocardial tissue area (TNC area). Clinical parameters associated with TNC area were investigated. The patients were divided into two groups based on receiver operating characteristic analysis of TNC area to predict death: high TNC group with TNC area ≥2.3% (22 patients) and low TNC group with TNC area <2.3% (101 patients). High TNC was associated with diabetes mellitus. Comparing echocardiographic findings between before and 9 months after endomyocardial biopsy, the low TNC group was associated with decreased LV end‐diastolic diameter and increased LV ejection fraction, whereas the high TNC group was not. Survival analysis revealed a worse outcome in the high TNC group than in the low TNC group (P < 0.001). Multivariable Cox regression analysis revealed that TNC area was independently associated with poor outcome (HR = 1.347, P = 0.032).ConclusionsIncreased myocardial TNC expression was associated with worse LV remodeling and long‐term outcome in DCM.

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Section: Discussionmentioning

confidence: 99%

Significance of myocardial tenascin‐C expression in left ventricular remodelling and long‐term outcome in patients with dilated cardiomyopathy

Yokokawa

Sugano

Nakayama

et al. 2016

European J of Heart Fail

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“…Other potential strategies targeting phosphodiesterase III, angiotensin II type 1 receptor (AT-1) and angiotensin converting enzyme (ACE) had already been described elsewhere 2,18,24 and therefore only will be briefly revisited here. Cilostazol inhibits phosphodiesterase III preventing tenascin-C expression by vascular smooth muscle cells during neointimal hyperplasia.…”

Section: Blocking Tenascin-c Inducing Signaling With Inhibitory Drugsmentioning

confidence: 99%

“…18,24 Irradiation also has an impact on the immune response and can trigger "cellular immunology." 82 In particular, a high-dose and few-fraction schedule had been reported to trigger inflammation associated apoptosis that was characterized by the recruitment of dendritic cells to the irradiated site.…”

Section: Induction Of Tenascin-c Upon Radiotherapymentioning

confidence: 99%

Tenascin-C: Exploitation and collateral damage in cancer management

Spenlé

Saupe

Midwood³

et al. 2015

Cell Adhesion & Migration

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“…One important feature of AT expansion and the subsequent accumulation of ECM components is AT hypoxia, which ultimately leads to fibrosis 17 . Tenascin C (TNC), which belongs to the damage-associated molecular patterns family, constitutes a large hexameric glycoprotein highly expressed where tissue structures are dramatically remodeled, including embryonic development, cancer invasion, or wound healing 18 . TNC is associated with tissue injury as well as inflammation and modulates fibrotic and inflammatory responses in diverse diseases, such as liver fibrosis, arthritis, or obesity by inducing the production of proinflammatory cytokines [19][20][21] .…”

Section: Introductionmentioning

confidence: 99%

Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C

et al. 2018

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Background/Objectives: Obesity is related to a dynamic extracellular matrix (ECM) remodeling, which involves the synthesis and degradation of different proteins, such as tenascin C (TNC) in the adipose tissue (AT). Given the functional relationship between leptin and inducible nitric oxide synthase (iNOS), our aim was to analyze the impact of the absence of the iNOS gene in AT inflammation and ECM remodeling in ob/ob mice. Subjects/Methods: The expression of genes involved in inflammation and ECM remodeling was evaluated in 10-week-old male double knockout (DBKO) mice simultaneously lacking the ob and iNOS genes as well as in ob/ob mice classified into three groups [control, leptin-treated (1 mg kg −1 day −1 ) and pair-fed]. Results: Leptin deficiency increased inflammation and fibrosis in AT. As expected, leptin treatment improved the obesity phenotype. iNOS deficiency in ob/ob mice improved insulin sensitivity, AT inflammation, and ECM remodeling, as evidenced by lower AT macrophage infiltration and collagen deposition, a downregulation of proinflammatory and profibrogenic genes Tnf, Emr1, Hif1a, Col6a1, Col6a3, and Tnc, as well as lower circulating TNC levels. Interestingly, leptin upregulated TNC expression and release in 3T3-L1 adipocytes, and iNOS knockdown in 3T3-L1 fat cells produced a significant decrease in basal and leptin-induced Tnc expression. Conclusions: Ablation of iNOS in leptin-deficient mice improved AT inflammation and ECM remodeling-related genes, attenuating fibrosis, and metabolic dysfunction. The activation of iNOS by leptin is necessary for the synthesis and secretion of TNC in adipocytes, suggesting an important role of this alarmin in the development of AT inflammation and fibrosis.

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Advances in tenascin-C biology

Cited by 274 publications

References 187 publications

Significance of myocardial tenascin‐C expression in left ventricular remodelling and long‐term outcome in patients with dilated cardiomyopathy

Significance of myocardial tenascin‐C expression in left ventricular remodelling and long‐term outcome in patients with dilated cardiomyopathy

Tenascin-C: Exploitation and collateral damage in cancer management

Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C

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