Angiotensin II Mobilizes Spleen Monocytes to Promote the Development of Abdominal Aortic Aneurysm in Apoe −/− Mice
Safa Mellak, Hafid Ait-Oufella, Bruno Esposito, Xavier Loyer, Maxime Poirier, Thomas F. Tedder, Alain Tedgui, Ziad Mallat et al.. Arteriosclerosis, Thrombosis, and Vascular Biology, 2015-02
Topic: Inflammation, microglia and astrocytes
Objective—: Abdominal aortic aneurysm (AAA) is widespread among elderly people and results in progressive expansion and rupture of the aorta with high mortality. Macrophages, which are the main population observed within the site of aneurysm, are thought to derive from circulating monocytes although no direct evidence has been provided to date. In this study, we were particularly interested in understanding the trafficking behavior of monocyte subsets in AAA and their role in disease pathogenesis. Approach and Results—: Using bone marrow transplantation in Apoe −/− mice, we showed that circulating monocytes give rise to abdominal aortic macrophages in hypercholesterolemic mice submitted to angiotensin II (AngII). Detailed monitoring of monocyte compartmentalization revealed that lymphocyte antigen 6C high and lymphocyte antigen 6C low monocytes transiently increase in blood early after AngII infusion and differentially infiltrate the abdominal aorta. The splenic reservoir accounted for the mobilization of the 2 monocyte subsets after 3 days of AngII infusion. Spleen removal or lymphocyte deficiency in Apoe −/− Rag2 −/− mice similarly impaired early monocyte increase in blood in response to AngII and protected against AAA development, independently of blood pressure. Reconstitution of Apoe −/− Rag2 −/− mice with total splenocytes but not with B-cell–depleted splenocytes restored monocyte mobilization in response to AngII and enhanced susceptibility to AAA. Conclusions—: Taken together, the data show that lymphocyte antigen 6C high and lymphocyte antigen 6C low monocytes are mobilized from the spleen in response to AngII. Intriguingly, the process is dependent on the presence of B cells and significantly contributes to the development of AAA and the occurrence of aortic rupture.
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APA 7th
Mellak, S., Ait-Oufella, H., Esposito, B., Loyer, X., Poirier, M., Tedder, T. F., et al. (2015). Angiotensin II Mobilizes Spleen Monocytes to Promote the Development of Abdominal Aortic Aneurysm in Apoe −/− Mice. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/atvbaha.114.304389
Vancouver
Mellak S, Ait-Oufella H, Esposito B, Loyer X, Poirier M, Tedder TF, et al. Angiotensin II Mobilizes Spleen Monocytes to Promote the Development of Abdominal Aortic Aneurysm in Apoe −/− Mice. Arteriosclerosis, Thrombosis, and Vascular Biology. 2015. doi:10.1161/atvbaha.114.304389.
BibTeX
@article{mellak2015-3e43caee,
author = {Mellak, Safa and Ait-Oufella, Hafid and Esposito, Bruno and Loyer, Xavier and Poirier, Maxime and Tedder, Thomas F. and Tedgui, Alain and Mallat, Ziad and others},
title = {{Angiotensin II Mobilizes Spleen Monocytes to Promote the Development of Abdominal Aortic Aneurysm in Apoe −/− Mice}},
journal = {Arteriosclerosis, Thrombosis, and Vascular Biology},
year = {2015},
doi = {10.1161/atvbaha.114.304389},
url = {https://doi.org/10.1161/atvbaha.114.304389}
}
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Key findings
- Objective—: Abdominal aortic aneurysm (AAA) is widespread among elderly people and results in progressive expansion and rupture of the aorta with high mortality.
- Approach and Results—: Using bone marrow transplantation in Apoe −/− mice, we showed that circulating monocytes give rise to abdominal aortic macrophages in hypercholesterolemic mice submitted to angiotensin II (AngII).
- Detailed monitoring of monocyte compartmentalization revealed that lymphocyte antigen 6C high and lymphocyte antigen 6C low monocytes transiently increase in blood early after AngII infusion and differentially infiltrate the abdominal aorta.
- Conclusions—: Taken together, the data show that lymphocyte antigen 6C high and lymphocyte antigen 6C low monocytes are mobilized from the spleen in response to AngII.
- Intriguingly, the process is dependent on the presence of B cells and significantly contributes to the development of AAA and the occurrence of aortic rupture.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 20 of the 56 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Arteriosclerosis, Thrombosis, and Vascular Biology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2015 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mice”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 20 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 20 of the 56 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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