The C57Bl/6J mouse strain is more susceptible to angiotensin II-induced aortic aneurysm formation than C57Bl/6N
Background and aims - Genetic variations between C57Bl/6 mouse substrains are highly relevant to the investigation of cardiovascular disease. We here assessed whether these variations have an impact on the incidence of abdominal aortic aneurysms (AAA) in C57Bl/6J and 6 N mice. - Methods - AAA were i...
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| Main Authors: | , , , , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
2021
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| In: |
Atherosclerosis
Year: 2020, Volume: 318, Pages: 8-13 |
| ISSN: | 1879-1484 |
| DOI: | 10.1016/j.atherosclerosis.2020.11.032 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.atherosclerosis.2020.11.032 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0021915020315525 |
| Author Notes: | Markus Wortmann, Muhammad Arshad, Andreas S. Peters, Maani Hakimi, Dittmar Böckler, Susanne Dihlmann |
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| 245 | 1 | 4 | |a The C57Bl/6J mouse strain is more susceptible to angiotensin II-induced aortic aneurysm formation than C57Bl/6N |c Markus Wortmann, Muhammad Arshad, Andreas S. Peters, Maani Hakimi, Dittmar Böckler, Susanne Dihlmann |
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| 520 | |a Background and aims - Genetic variations between C57Bl/6 mouse substrains are highly relevant to the investigation of cardiovascular disease. We here assessed whether these variations have an impact on the incidence of abdominal aortic aneurysms (AAA) in C57Bl/6J and 6 N mice. - Methods - AAA were induced by subcutaneous infusion of 1500 ng/kg*min Angiotensin-II for four weeks in six-month-old male CB57Bl/6J and 6N mice. Aortic smooth muscle cells (VSMC) were isolated from untreated animals for in vitro analysis. - Results - C57Bl/6J mice are more susceptible to AAA formation (76.5% vs. 7.1%, p = 0.0002). C57Bl/6J VSMC expressed more pro-inflammatory molecules such as Nlrp3, Aim2 and NF-κB. Additionally, these cells presented significantly higher levels of NADP/NADPH and oxidative DNA modifications, as indicated by 8-OHdG-staining, compared to C57Bl/6N VSMC. - Conclusions - In contrast to previous reports, we present evidence that six-month-old C57BL/6J, but not C57BL/6N mice develop AAA. In accordance with the deficiency of nicotinamide-nucleotide-transhydrogenase (Nnt), C57BL/6J VSMC displayed increased oxidative stress, oxidative DNA damage and a stronger inflammatory phenotype than C57BL/6N VSMC. | ||
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| 650 | 4 | |a Angiotensin II | |
| 650 | 4 | |a Aortic aneurysm | |
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| 650 | 4 | |a C57Bl/6N | |
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