Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice

Tomohiro Nishioka, Katsuya Onishi, Naoshi Shimojo, Yuka Nagano, Hidenori Matsusaka, Masaki Ikeuchi, Tomomi Ide, Hiroyuki Tsutsui, Michiaki Hiroe, Toshimichi Yoshida, Kyoko Imanaka-Yoshida

Research output: Contribution to journalArticlepeer-review

97 Citations (Scopus)


Tenascin-C (TN-C) is an extracellular matrix glycoprotein with high bioactivity. It is expressed at low levels in normal adult heart, but upregulated under pathological conditions, such as myocardial infarction (MI). Recently, we (Ref. 34) reported that MI patients with high serum levels of TN-C have a greater incidence of maladaptive cardiac remodeling and a worse prognosis. We hypothesized that TN-C may aggravate left ventricular remodeling. To examine the effects of TN-C, MI was induced by ligating coronary arteries of TN-C knockout (KO) mice under anesthesia and comparing them with sibling wild-type (WT) mice. In WT+MI mice, TN-C expression was upregulated at day 1, peaked at day 5, downregulated and disappeared by day 28, and the molecule was localized in the border zone between intact myocardium and infarct lesions. The morphometrically determined infarct size and survival rate on day 28 were comparable between the WT+MI and KO+MI groups. Echocardiography and hemodynamic analyses demonstrated left ventricular end-diastolic diameter, myocardial stiffness, and left ventricular end-diastolic pressure to be significantly increased in both WT+MI and KO+MI mice compared with sham-operated mice. However, end-diastolic pressure and dimension and myocardial stiffness of KO+MI were lower than those of the WT+MI mice. Histological examination revealed normal tissue healing, but interstitial fibrosis in the residual myocardium in peri-infarcted areas was significantly less pronounced in KO+MI mice than in WT+MI mice. TN-C may thus accelerate adverse ventricular remodeling, cardiac failure, and fibrosis in the residual myocardium after MI.

Original languageEnglish
Pages (from-to)H1072-H1078
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number3
Publication statusPublished - Mar 2010

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


Dive into the research topics of 'Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice'. Together they form a unique fingerprint.

Cite this