Academic Journal
Administration of anti-inflammatory M2 macrophages suppresses progression of angiotensin II-induced aortic aneurysm in mice
العنوان: | Administration of anti-inflammatory M2 macrophages suppresses progression of angiotensin II-induced aortic aneurysm in mice |
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المؤلفون: | Ashida, Shinichi, Yamawaki-Ogata, Aika, Tokoro, Masayoshi, Mutsuga, Masato, Usui, Akihiko, Narita, Yuji |
المساهمون: | The Japan Society for the Promotion of Science (JSPS) KAKENHI |
المصدر: | Scientific Reports ; volume 13, issue 1 ; ISSN 2045-2322 |
بيانات النشر: | Springer Science and Business Media LLC |
سنة النشر: | 2023 |
الوصف: | Aortic aneurysm (AA) is a vascular disorder characterized pathologically by inflammatory cell invasion and extracellular matrix (ECM) degradation. It is known that regulation of the balance between pro-inflammatory M1 macrophages (M1Ms) and anti-inflammatory M2 macrophages (M2Ms) plays a pivotal role in AA stabilization. We investigated the effects of M2M administration in an apolipoprotein E-deficient (apoE −/− ) mouse model in which AA was induced by angiotensin II (ATII) infusion. Mice received intraperitoneal administration of 1 million M2Ms 4 weeks after ATII infusion. Compared with a control group that was administered saline, the M2M group exhibited reduced AA expansion; decreased expression levels of interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1); and a lower M1M/M2M ratio. Moreover, the M2M group exhibited upregulation of anti-inflammatory factors, including IL-4 and IL-10. PKH26-labeled M2Ms accounted for 6.5% of cells in the aneurysmal site and co-expressed CD206. Taken together, intraperitoneal administration of M2Ms inhibited AA expansion by reducing the inflammatory reaction via regulating the M1M/M2M ratio. This study shows that M2M administration might be useful for the treatment of AA. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
DOI: | 10.1038/s41598-023-27412-x |
الاتاحة: | http://dx.doi.org/10.1038/s41598-023-27412-x https://www.nature.com/articles/s41598-023-27412-x.pdf https://www.nature.com/articles/s41598-023-27412-x |
Rights: | https://creativecommons.org/licenses/by/4.0 ; https://creativecommons.org/licenses/by/4.0 |
رقم الانضمام: | edsbas.FAB62502 |
قاعدة البيانات: | BASE |
DOI: | 10.1038/s41598-023-27412-x |
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