| Autor: |
Daiju Fukuda, Sachiko Nishimoto, Kunduziayi Aini, Atsushi Tanaka, Tsuyoshi Nishiguchi, Joo‐ri Kim‐Kaneyama, Xiao‐Feng Lei, Kiyoshi Masuda, Takuya Naruto, Kimie Tanaka, Yasutomi Higashikuni, Yoichiro Hirata, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Issei Imoto, Takashi Akasaka, Michio Shimabukuro, Masataka Sata |
| Jazyk: |
angličtina |
| Rok vydání: |
2019 |
| Předmět: |
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| Zdroj: |
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 8, Iss 7 (2019) |
| Druh dokumentu: |
article |
| ISSN: |
2047-9980 |
| DOI: |
10.1161/JAHA.118.010860 |
| Popis: |
Background Toll‐like receptor (TLR) 9 recognizes bacterial DNA, activating innate immunity, whereas it also provokes inflammation in response to fragmented DNA released from mammalian cells. We investigated whether TLR9 contributes to the development of vascular inflammation and atherogenesis using apolipoprotein E–deficient (Apoe−/−) mice. Methods and Results Tlr9‐deficient Apoe−/− (Tlr9−/−Apoe−/−) mice and Apoe−/− mice on a Western‐type diet received subcutaneous angiotensin II infusion (1000 ng/kg per minute) for 28 days. Angiotensin II increased the plasma level of double‐stranded DNA, an endogenous ligand of TLR9, in these mice. Genetic deletion or pharmacologic blockade of TLR9 in angiotensin II–infused Apoe−/− mice attenuated atherogenesis in the aortic arch (P |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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