The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Angiotensin-Converting Enzyme Inhibition Prevents the Release of Monocytes From Their Splenic Reservoir in Mice With Myocardial Infarction
Open accessAbstract
Rationale: Monocytes recruited to ischemic myocardium originate from a reservoir in the spleen, and the release from their splenic niche relies on angiotensin (Ang) II signaling. Objective: Because monocytes are centrally involved in tissue repair after ischemia, we hypothesized that early angiotensin-converting enzyme (ACE) inhibitor therapy impacts healing after myocardial infarction partly via effects on monocyte traffic. Methods and Results: In a mouse model of permanent coronary ligation, enalapril arrested the release of monocytes from the splenic reservoir and consequently reduced their recruitment into the healing infarct by 45%, as quantified by flow cytometry of digested infarcts. Time-lapse intravital microscopy revealed that enalapril reduces monocyte motility in the spleen. In vitro migration assays and Western blotting showed that this was caused by reduced signaling through the Ang II type 1 receptor. We then studied the long-term consequences of blocked splenic monocyte release in atherosclerotic apolipoprotein (apo)E −/− mice, in which infarct healing is impaired because of excessive inflammation in the cardiac wound. Enalapril improved histologic healing biomarkers and reduced inflammation in infarcts measured by FMT-CT (fluorescence molecular tomography in conjunction with x-ray computed tomography) of proteolytic activity. ACE inhibition improved MRI-derived ejection fraction by 14% on day 21, despite initially comparable infarct size. In apoE −/− mice, ischemia/reperfusion injury resulted in larger infarct size and enhanced monocyte recruitment and was reversible by enalapril treatment. Splenectomy reproduced antiinflammatory effects of enalapril. Conclusion: This study suggests that benefits of early ACE inhibition after myocardial infarction can partially be attributed to its potent antiinflammatory impact on the splenic monocyte reservoir.
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Cites
Inflammation in atherosclerosis
Libby, P. (2002) · Nature · doi:10.1038/nature01323 · Cited by 8,315
Pfeffer, M. A., Braunwald, E., Moyé, L. A., Basta, L., Brown, E. J., Cuddy, T. E., Davis, B. R., Geltman, E. M., Goldman, S., Flaker, G. C., et al. (1992) · New England Journal of Medicine · doi:10.1056/nejm199209033271001 · Cited by 5,911
Heart Disease and Stroke Statistics—2010 Update: A Report From the American Heart Association
WRITING GROUP MEMBERS, Lloyd-Jones, D., Adams, R. J., Brown, T. M., Carnethon, M., Dai, S., De Simone, G., Ferguson, T. B., Ford, E., Furie, K., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.192667 · Cited by 5,700
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Self-citationIdentification of splenic reservoir monocytes and their deployment to inflammatory sites
Swirski, F. K., Nahrendorf, M., Etzrodt, M., Wildgruber, M., Cortez-Retamozo, V., Panizzi, P., Figueiredo, J.-L., Kohler, R. H., Chudnovskiy, A., Waterman, P., et al. (2009) · Science · doi:10.1126/science.1175202 · Cited by 2,221
Self-citationImmune cell migration in inflammation: present and future therapeutic targets
Luster, A. D., Alon, R., & von Andrian, U. H. (2005) · Nature Immunology · doi:10.1038/ni1275 · Cited by 1,313
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Self-Renewing Resident Cardiac Macrophages Limit Adverse Remodeling Following Myocardial Infarction
Dick, S. A., Macklin, J. A., Nejat, S., Momen, A., Clemente-Casares, X., Althagafi, M. G., Chen, J., Kantores, C., Hosseinzadeh, S., Aronoff, L., et al. (2019) · Nature Immunology · doi:10.1038/s41590-018-0272-2 · Cited by 883
Therapeutic siRNA silencing in inflammatory monocytes in mice
Leuschner, F., Dutta, P., Gorbatov, R., Novobrantseva, T. I., Donahoe, J. S., Courties, G., Lee, K. M., Kim, J. I., Markmann, J. F., Marinelli, B., et al. (2011) · Nature Biotechnology · doi:10.1038/nbt.1989 · Cited by 839
Self-citationExtramedullary Hematopoiesis Generates Ly-6C high Monocytes That Infiltrate Atherosclerotic Lesions
Robbins, C. S., Chudnovskiy, A., Rauch, P. J., Figueiredo, J.-L., Iwamoto, Y., Gorbatov, R., Etzrodt, M., Weber, G. F., Ueno, T., van Rooijen, N., et al. (2012) · Circulation · doi:10.1161/circulationaha.111.061986 · Cited by 482
Self-citationInflammatory processes in cardiovascular disease: a route to targeted therapies
Ruparelia, N., Chai, J. T., Fisher, E. A., & Choudhury, R. P. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2016.185 · Cited by 477
Ma, Y., Mouton, A. J., & Lindsey, M. L. (2018) · Translational Research · doi:10.1016/j.trsl.2017.10.001 · Cited by 405
Metadata
- Authors
- Leuschner, F., Panizzi, P., Chico-Calero, I., Lee, W. W., Ueno, T., Cortez-Retamozo, V., Waterman, P., Gorbatov, R., Marinelli, B., Iwamoto, Y., Chudnovskiy, A., Figueiredo, J.-L., Sosnovik, D. E., Pittet, M. J., Swirski, F. K., Weissleder, R., & Nahrendorf, M.
- Venue
- Circulation Research
- Published
- 2010-11-26
- Volume
- 107
- Issue
- 11
- Pages
- 1364-1373
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2162787683
- Cited by
- 220
- References
- 6
- FWCI
- 9.20
- Type
- journal article
- Language
- en
- Open access
- bronze
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- The paper
- Leuschner, F., Panizzi, P., Chico-Calero, I., Lee, W. W., Ueno, T., Cortez-Retamozo, V., Waterman, P., Gorbatov, R., Marinelli, B., Iwamoto, Y., Chudnovskiy, A., Figueiredo, J.-L., Sosnovik, D. E., Pittet, M. J., Swirski, F. K., Weissleder, R., & Nahrendorf, M. (2010). Angiotensin-Converting Enzyme Inhibition Prevents the Release of Monocytes From Their Splenic Reservoir in Mice With Myocardial Infarction. Circulation Research. https://doi.org/10.1161/circresaha.110.227454
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
