HISTOLOGY AND HISTOPATHOLOGY

Cellular and Molecular Biology

 

Review

 

Interaction between cell and extracellular matrix in heart disease: Multiple roles of tenascin-C in tissue remodeling

K. Imanaka-Yoshida1, M. Hiroe2 and T. Yoshida1

1Department of Pathology, Mie University School of Medicine, Tsu, Japan and 2Department of Nephrology and Cardiology, International Medical Center of Japan, Tokyo, Japan

Offprint requests to: Dr. Kyoko Imanaka-Yoshida, Department of Pathology, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. Fax: +81-59-231-5210. e-mail: imanaka@doc.medic.mie.u.ac.jp

 

Summary. The heart remodels myocardial tissue in physiological and pathological response. The cell-extracellular matrix (ECM) interaction provides not only structural and mechanical support but also important biological signaling during tissue remodeling. Among various ECM molecules, tenascin-C (TNC) is well known as a regulator of multiple cellular functions during embryogenesis, wound healing or cancer progression. In the heart, TNC appears in several important steps of embryonic development such as the initial differentiation of cardiomyocytes or coronary vasculo/angiogenesis, but it is not detected in a normal adult myocardium. However, TNC is found to re-express after myocardial injury and may regulate cellular behavior during tissue remodeling by modulating the attachment of cardiomyocytes to connective tissue, by enhancing migration and differentiation of myofibroblasts, and by inducing matrix metallo-proteinases. TNC also interacts with other ECM molecules and may modulate progression of fibrosis. Furthermore, transient and site specific expression of TNC closely associated with myocardial injury and inflammation suggests not only its key roles during tissue remodeling but also that TNC can be a marker for myocardial disease activity. Histol. Histopathol. 19, 517-525 (2004)

Key words: Tenascin-C, Extracellular matrix, Remodeling, Fibrosis, Myocarditis, Myocardial infarction

DOI: 10.14670/HH-19.517