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Miller HA, Schake MA, Bony BA, et al. Smooth muscle cells affect differential nanoparticle accumulation in disturbed blood flow-induced murine atherosclerosis. PLoS One. 2021;16(12):e0260606doi: 10.1371/journal.pone.0260606.
Miller, H. A., Schake, M. A., Bony, B. A., Curtis, E. T., Gee, C. C., McCue, I. S., Ripperda, T. J., Chatzizisis, Y. S., Kievit, F. M., & Pedrigi, R. M. (2021). Smooth muscle cells affect differential nanoparticle accumulation in disturbed blood flow-induced murine atherosclerosis. PloS one, 16(12), e0260606. https://doi.org/10.1371/journal.pone.0260606
Miller, Hunter A, et al. "Smooth muscle cells affect differential nanoparticle accumulation in disturbed blood flow-induced murine atherosclerosis." PloS one vol. 16,12 (2021): e0260606. doi: https://doi.org/10.1371/journal.pone.0260606
Miller HA, Schake MA, Bony BA, Curtis ET, Gee CC, McCue IS, Ripperda TJ, Chatzizisis YS, Kievit FM, Pedrigi RM. Smooth muscle cells affect differential nanoparticle accumulation in disturbed blood flow-induced murine atherosclerosis. PLoS One. 2021 Dec 09;16(12):e0260606. doi: 10.1371/journal.pone.0260606. eCollection 2021. PMID: 34882722; PMCID: PMC8659666.
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PLoS One. 2021 Dec 09;16(12):e0260606. doi: 10.1371/journal.pone.0260606. eCollection 2021.

Smooth muscle cells affect differential nanoparticle accumulation in disturbed blood flow-induced murine atherosclerosis.

PloS one

Hunter A Miller, Morgan A Schake, Badrul Alam Bony, Evan T Curtis, Connor C Gee, Ian S McCue, Thomas J Ripperda, Yiannis S Chatzizisis, Forrest M Kievit, Ryan M Pedrigi

Affiliations

  1. Department of Biological Systems Engineering, University of Nebraska-Lincoln, Lincoln, NE, United States of America.
  2. Department of Mechanical and Materials Engineering, University of Nebraska-Lincoln, Lincoln, NE, United States of America.
  3. Cardiovascular Division, University of Nebraska Medical Center, Omaha, NE, United States of America.

PMID: 34882722 PMCID: PMC8659666 DOI: 10.1371/journal.pone.0260606

Abstract

Atherosclerosis is a lipid-driven chronic inflammatory disease that leads to the formation of plaques in the inner lining of arteries. Plaques form over a range of phenotypes, the most severe of which is vulnerable to rupture and causes most of the clinically significant events. In this study, we evaluated the efficacy of nanoparticles (NPs) to differentiate between two plaque phenotypes based on accumulation kinetics in a mouse model of atherosclerosis. This model uses a perivascular cuff to induce two regions of disturbed wall shear stress (WSS) on the inner lining of the instrumented artery, low (upstream) and multidirectional (downstream), which, in turn, cause the development of an unstable and stable plaque phenotype, respectively. To evaluate the influence of each WSS condition, in addition to the final plaque phenotype, in determining NP uptake, mice were injected with NPs at intermediate and fully developed stages of plaque growth. The kinetics of artery wall uptake were assessed in vivo using dynamic contrast-enhanced magnetic resonance imaging. At the intermediate stage, there was no difference in NP uptake between the two WSS conditions, although both were different from the control arteries. At the fully-developed stage, however, NP uptake was reduced in plaques induced by low WSS, but not multidirectional WSS. Histological evaluation of plaques induced by low WSS revealed a significant inverse correlation between the presence of smooth muscle cells and NP accumulation, particularly at the plaque-lumen interface, which did not exist with other constituents (lipid and collagen) and was not present in plaques induced by multidirectional WSS. These findings demonstrate that NP accumulation can be used to differentiate between unstable and stable murine atherosclerosis, but accumulation kinetics are not directly influenced by the WSS condition. This tool could be used as a diagnostic to evaluate the efficacy of experimental therapeutics for atherosclerosis.

Conflict of interest statement

The authors have declared that no competing interests exist.

References

  1. ACS Nano. 2015 Feb 24;9(2):1837-47 - PubMed
  2. ACS Nano. 2019 Dec 24;13(12):13759-13774 - PubMed
  3. Contrast Media Mol Imaging. 2011 Jan-Feb;6(1):35-45 - PubMed
  4. Circulation. 1992 Dec;86(6 Suppl):III30-42 - PubMed
  5. Circulation. 2004 Oct 5;110(14):2032-8 - PubMed
  6. Circulation. 2011 Aug 16;124(7):779-88 - PubMed
  7. JACC Cardiovasc Imaging. 2013 Oct;6(10):1108-1114 - PubMed
  8. Cardiovasc Res. 2013 Jul 15;99(2):315-27 - PubMed
  9. J Am Coll Cardiol. 2007 Jun 26;49(25):2379-93 - PubMed
  10. Biomater Sci. 2014 Sep 29;2(9):1287-1295 - PubMed
  11. Circulation. 2012 Jul 10;126(2):172-81 - PubMed
  12. Sci Rep. 2019 Nov 6;9(1):16099 - PubMed
  13. Blood. 2009 Jan 8;113(2):438-46 - PubMed
  14. EuroIntervention. 2018 Nov 20;14(10):1129-1135 - PubMed
  15. Arterioscler Thromb Vasc Biol. 2013 Feb;33(2):249-56 - PubMed
  16. Curr Cardiovasc Imaging Rep. 2011 Aug;4(4):276-283 - PubMed
  17. Nat Rev Drug Discov. 2011 Oct 21;10(11):835-52 - PubMed
  18. Circulation. 2015 Sep 15;132(11):1003-12 - PubMed
  19. Hum Pathol. 1995 Apr;26(4):450-6 - PubMed
  20. Circ Cardiovasc Imaging. 2016 Dec;9(12): - PubMed
  21. Proc Natl Acad Sci U S A. 2017 Jul 3;114(27):6960-6965 - PubMed
  22. Int J Inflam. 2011;2011:936109 - PubMed
  23. Cardiovasc Res. 2013 Jul 15;99(2):334-41 - PubMed
  24. Circulation. 2006 Jun 13;113(23):2744-53 - PubMed
  25. Dalton Trans. 2017 Sep 26;46(37):12692-12704 - PubMed
  26. J Control Release. 2019 Oct;311-312:245-256 - PubMed
  27. Theranostics. 2018 Apr 3;8(9):2521-2548 - PubMed
  28. Circulation. 2011 Feb 15;123(6):621-30 - PubMed
  29. J Vasc Surg. 2007 Jan;45(1):155-9 - PubMed
  30. Proc Natl Acad Sci U S A. 2016 Nov 1;113(44):E6731-E6740 - PubMed
  31. Circ Cardiovasc Interv. 2019 Jul;12(7):e007791 - PubMed
  32. Eur Heart J. 2013 Mar;34(10):719-28 - PubMed
  33. J Mol Cell Cardiol. 2015 Dec;89(Pt B):168-72 - PubMed
  34. Biomaterials. 2008 Feb;29(4):487-96 - PubMed
  35. Arterioscler Thromb Vasc Biol. 2000 May;20(5):1262-75 - PubMed
  36. Adv Mater. 2019 Feb;31(8):e1804567 - PubMed
  37. J Am Coll Cardiol. 2014 Apr 1;63(12):1134-1140 - PubMed
  38. Cell Res. 2017 Mar;27(3):352-372 - PubMed
  39. Vascul Pharmacol. 2015 Nov;74:103-113 - PubMed
  40. R Soc Open Sci. 2016 Oct 19;3(10):160588 - PubMed
  41. Circulation. 2008 Feb 26;117(8):993-1002 - PubMed
  42. Atherosclerosis. 2015 Aug;241(2):772-82 - PubMed
  43. Nanomedicine (Lond). 2008 Oct;3(5):703-17 - PubMed
  44. J Mater Chem B. 2014 Apr 28;2(16):2240-2247 - PubMed
  45. Atherosclerosis. 2015 Nov;243(1):1-10 - PubMed
  46. Biomaterials. 2014 Feb;35(5):1636-42 - PubMed
  47. ACS Omega. 2020 Jun 23;5(26):16220-16227 - PubMed

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