Tenascin expression in endomyocardial biopsy specimens in patients with dilated cardiomyopathy: distribution along margin of fibrotic lesions.

Abstract

Objective-To examine the hypothesis that tenascin, an extracellular matrix glycoprotein, contributes to fibrotic changes in dilated cardiomyopathy. Methods-The localisation of tenascin in biopsy specimens of the hearts obtained from eight patients with dilated cardiomyopathy was examined using staining by the avidin-biotin-peroxidase complex methodResults-(1) Perimysium and endomysium. Although positive staining for tenascin was observed in the enlarged perimysium and endomysium in all patients, moderately intense staining was characteristically observed near the replacement fibrotic lesions. In the narrow perimysium and endomysium of the myocardium not containing replacement fibrotic lesions, tenascin was not present, as in the control specimens. (2) Replacement fibrotic lesions. Non-homogeneous positive staining for tenascin was detected in all replacement fibrotic lesions examined. Intense tenascin deposition was observed in the peripheral portion of the replacement fibrotic lesions. The tenascin staining observed in the small replacement fibrotic lesions was more intense than that in the large lesions. Conclusions-Tenascin contributes to the development of the fibrotic changes seen in the dilated cardiomyopathic heart. Its characteristic location, specifically the distribution along the margin of the fibrosis, suggests that fibrotic change is a continuous process in hearts with dilated cardiomyopathy.

Higher Serum Tenascin-C Levels Reflect the Severity of Heart Failure, Left Ventricular Dysfunction and Remodeling in Patients With Dilated Cardiomyopathy

“…The origin of the elevated level of circulating TN-C in DCM is a matter of interest. It has been reported that expression of TN-C is observed in endomyocardial biopsy specimens of patients with DCM, 27 which strongly suggests that the serum TN-C arises from heart tissue. In the pathological myocardium, results obtained from experimental animal models, as well as human myocarditis samples, have identified that the major source of TN-C is interstitial fibroblasts.…”

Tenascin-C in cardiovascular remodeling: potential impact for diagnosis, prognosis estimation and targeted therapy

“…29 At the same time, a re-expression of tenascin in cardiac biopsies of DCM patients with a distribution pattern along the margins of fibrotic areas could be observed. 30 Some years later, the first reports occurred on significantly elevated tenascin-C serum levels in patients suffering from DCM. Aso and co-workers could demonstrate higher circulating tenascin-C levels in patients with DCM compared to controls.…”

Pressure Overload-induced Right Ventricular Failure is Associated with Re-expression of Myocardial Tenascin-C and Elevated Plasma Tenascin-C Levels

“…TNC is re-expressed during wound healing, inflammation, regeneration, and cancer invasion [1]. In the heart, TNC is primarily expressed during cardiogenesis but reappears in the adult myocardium under various pathological conditions, including acute myocardial infarction (AMI) [2], myocarditis [3], and dilated cardiomyopathy [4]. Elevated serum levels of TNC may reflect re-expression of TNC in myocardial tissue, and the specific pathological expression pattern of myocardial TNC suggests that plasma TNC levels may be useful as a marker of left ventricular remodeling in patients with AMI, dilated cardiomyopathy or heart failure [5][6][7].…”