Activation of an Innate Immune Receptor, Nod1, Accelerates Atherogenesis in Apoe −/− Mice
Shunsuke Kanno, Hisanori Nishio, Tamami Tanaka, Yoshitomo Motomura, Kenji Murata, Kenji Ihara, Mitsuho Onimaru, Sho Yamasaki et al.. The Journal of Immunology, 2015-01
Topic: Inflammation, microglia and astrocytes
Atherosclerosis is essentially a vascular inflammatory process in the presence of an excess amount of lipid. We have recently reported that oral administration of a nucleotide-binding oligomerization domain (Nod)-1 ligand, FK565, induced vascular inflammation in vivo. No studies, however, have proven the association between Nod1 and atherosclerosis in vivo. To investigate a potential role of NOD1 in atherogenesis, we orally administered FK565 to apolipoprotein E knockout (Apoe−/−) mice for 4 wk intermittently and performed quantification of atherosclerotic lesions in aortic roots and aortas, immunohistochemical analyses, and microarray-based gene expression profiling of aortic roots. FK565 administration accelerated the development of atherosclerosis in Apoe−/− mice, and the effect was dependent on Nod1 in non–bone marrow origin cells by bone marrow transplantation experiments. Immunohistochemical studies revealed the increases in the accumulation of macrophages and CD3 T cells within the plaques in aortic roots. Gene expression analyses of aortic roots demonstrated a marked upregulation of the Ccl5 gene during early stage of atherogenesis, and the treatment with Ccl5 antagonist significantly inhibited the acceleration of atherosclerosis in FK565-administered Apoe−/− mice. Additionally, as compared with Apoe−/− mice, Apoe and Nod1 double-knockout mice showed reduced development of atherosclerotic lesions from the early stage as well as their delayed progression and a significant reduction in Ccl5 mRNA levels at 9 wk of age. Data in the present study show that the Nod1 signaling pathway in non–bone marrow-derived cells contributes to the development of atherosclerosis.
Key findings
- Immunohistochemical studies revealed the increases in the accumulation of macrophages and CD3 T cells within the plaques in aortic roots.
- Gene expression analyses of aortic roots demonstrated a marked upregulation of the Ccl5 gene during early stage of atherogenesis, and the treatment with Ccl5 antagonist significantly inhibited the acceleration of atherosclerosis in FK565-administered Apoe−/− mice.
- Additionally, as compared with Apoe−/− mice, Apoe and Nod1 double-knockout mice showed reduced development of atherosclerotic lesions from the early stage as well as their delayed progression and a significant reduction in Ccl5 mRNA levels at 9 wk of age.
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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 (The Journal of Immunology) |
| 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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APA 7th
Kanno, S., Nishio, H., Tanaka, T., Motomura, Y., Murata, K., Ihara, K., et al. (2015). Activation of an Innate Immune Receptor, Nod1, Accelerates Atherogenesis in Apoe −/− Mice. The Journal of Immunology. https://doi.org/10.4049/jimmunol.1302841
Vancouver
Kanno S, Nishio H, Tanaka T, Motomura Y, Murata K, Ihara K, et al. Activation of an Innate Immune Receptor, Nod1, Accelerates Atherogenesis in Apoe −/− Mice. The Journal of Immunology. 2015. doi:10.4049/jimmunol.1302841.
BibTeX
@article{kanno2015-6b92c190,
author = {Kanno, Shunsuke and Nishio, Hisanori and Tanaka, Tamami and Motomura, Yoshitomo and Murata, Kenji and Ihara, Kenji and Onimaru, Mitsuho and Yamasaki, Sho and others},
title = {{Activation of an Innate Immune Receptor, Nod1, Accelerates Atherogenesis in Apoe −/− Mice}},
journal = {The Journal of Immunology},
year = {2015},
doi = {10.4049/jimmunol.1302841},
url = {https://doi.org/10.4049/jimmunol.1302841}
}
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