Abstract | BACKGROUND:
Tenascin-C (TN-C), an extracellular matrix glycoprotein, appears at several important steps of cardiac development in the embryo, but is sparse in the normal adult heart. TN-C re-expresses under pathological conditions including myocarditis, and is closely associated with tissue injury and inflammation in both experimental and clinical settings. However, the pathophysiological role of TN-C in the development of myocarditis is not clear. We examined how TN-C affects the initiation of experimental autoimmune myocarditis, immunologically. METHODS AND RESULTS: CONCLUSIONS: Our results demonstrated that TN-C aggravates autoimmune myocarditis by driving the dendritic cell activation and Th17 differentiation via Toll-like receptor 4. The blockade of Toll-like receptor 4-mediated signaling to inhibit the proinflammatory effects of TN-C could be a promising therapeutic strategy against autoimmune myocarditis.
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Authors | Tomoko Machino-Ohtsuka, Kazuko Tajiri, Taizo Kimura, Satoshi Sakai, Akira Sato, Toshimichi Yoshida, Michiaki Hiroe, Yasuhiro Yasutomi, Kazutaka Aonuma, Kyoko Imanaka-Yoshida |
Journal | Journal of the American Heart Association
(J Am Heart Assoc)
Vol. 3
Issue 6
Pg. e001052
(Nov 05 2014)
ISSN: 2047-9980 [Electronic] England |
PMID | 25376187
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. |
Chemical References |
- Inflammation Mediators
- Interleukin-6
- Myh6 protein, mouse
- Tenascin
- Tlr4 protein, mouse
- Toll-Like Receptor 4
- interleukin-6, mouse
- Myosin Heavy Chains
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Topics |
- Animals
- Autoimmune Diseases
(genetics, immunology, metabolism, physiopathology)
- Cell Differentiation
- Cells, Cultured
- Coculture Techniques
- Dendritic Cells
(immunology, metabolism)
- Disease Models, Animal
- Inflammation Mediators
(immunology, metabolism)
- Interleukin-6
(immunology, metabolism)
- Male
- Mice, Inbred BALB C
- Mice, Knockout
- Myocarditis
(genetics, immunology, metabolism, physiopathology)
- Myocardium
(immunology, metabolism)
- Myosin Heavy Chains
(immunology)
- Signal Transduction
- Tenascin
(deficiency, genetics, metabolism)
- Th17 Cells
(immunology, metabolism)
- Time Factors
- Toll-Like Receptor 4
(genetics, immunology, metabolism)
- Ventricular Function, Left
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