Abstract 385: Tenascin-C Worsens Myocardial Inflammation and Fibrosis by Enhancing Macrophage Activation via NF-kappaB in Mouse Hypertensive Heart

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2013-09, Vol.62 (suppl_1)
• Main Authors: Shimojo, Naoshi, Hashizume, Ryotaro, Hara, Mari, Suzuki, Yuka, Nishioka, Tomohiro, Yoshida, Toshimichi, Imanaka-Yoshida, Kyoko
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.62.suppl_1.A385

Abstract only Background and Aim: Tenascin-C (TN-C) is an extracellular matrix glycoprotein, not detected in normal adult heart but it expresses under various pathological conditions. We have previously reported in the enhanced TN-C production and accumulation of macrophages in the perivascular lesions of angiotensin II (AgII)-induced cardiac fibrosis mouse model. To clarify the role of TN-C in molecular mechanism, we analyzed the effect of TN-C in hypertensive heart utilizing wild-type (WT) and TN-C knock-out (TNKO) mice. Furthermore, to assess whether TN-C is involved in macrophage activation, we investigated in vitro study using macrophages isolated from the peritoneal cavity of WT mice. Methods and Results: Balb/c WT and TNKO mice were treated with 560 ng/kg body weight/min AgII subcutaneously by osmotic minipump for 4 weeks (WT/AgII and TNKO/AgII), and analyzed histological and molecular biological approaches. AgII treatment increased blood pressure, heart weight/body weight ratio, atrial and brain natriuretic peptide expression level and sizes of cardiomyocytes, but no significant differences were detected between WT/AgII and TNKO/AgII mice. In WT/AgII mice, interstitial collagen fibers (10.29±5.09% vs. WT: 4.6±1.56%, p