Tenascin C protects aorta from acute dissection in mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-05

AUTHORS

Taizo Kimura, Kozoh Shiraishi, Aya Furusho, Sohei Ito, Saki Hirakata, Norifumi Nishida, Koichi Yoshimura, Kyoko Imanaka-Yoshida, Toshimichi Yoshida, Yasuhiro Ikeda, Takanobu Miyamoto, Takafumi Ueno, Kimikazu Hamano, Michiaki Hiroe, Kazutaka Aonuma, Masunori Matsuzaki, Tsutomu Imaizumi, Hiroki Aoki

ABSTRACT

Acute aortic dissection (AAD) is caused by the disruption of intimomedial layer of the aortic walls, which is immediately life-threatening. Although recent studies indicate the importance of proinflammatory response in pathogenesis of AAD, the mechanism to keep the destructive inflammatory response in check is unknown. Here, we report that induction of tenascin-C (TNC) is a stress-evoked protective mechanism against the acute hemodynamic and humoral stress in aorta. Periaortic application of CaCl₂ caused stiffening of abdominal aorta, which augmented the hemodynamic stress and TNC induction in suprarenal aorta by angiotensin II infusion. Deletion of Tnc gene rendered mice susceptible to AAD development upon the aortic stress, which was accompanied by impaired TGFβ signaling, insufficient induction of extracellular matrix proteins and exaggerated proinflammatory response. Thus, TNC works as a stress-evoked molecular damper to maintain the aortic integrity under the acute stress. More... »

PAGES

4051

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep04051

DOI

http://dx.doi.org/10.1038/srep04051

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1040669278

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24514259


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