Print Email Facebook Twitter StemBell therapy stabilizes atherosclerotic plaques after myocardial infarction Title StemBell therapy stabilizes atherosclerotic plaques after myocardial infarction Author Woudstra, L. Meinster, E. van Haren, L. Kay, A.M. Kooman, M. Belien, J.A.M. Morrison, M.C. van Rossum, A.C. Helder, M.N. Juffermans, J.M. Niessen, H.W.M. Krijnen, P.A.J. Publication year 2018 Abstract Background aims. After a myocardial infarction (MI) atherosclerosis is accelerated leading to destabilization of the atherosclerotic plaque. mesenchymal stromal cells are a promising therapeutic option for atherosclerosis. Previously, we demonstrated a novel stem cell delivery technique, with adipose stem cells coupled to microbubbles (i.e., StemBells) as therapy after MI. In this study, we aim to investigate the effect of StemBell therapy on atherosclerotic plaques in an atherosclerotic mouse model after MI. Methods. MI was induced in atherosclerotic Apolipoprotein E–deficient mice that were fed a high-fat Western diet. Six days post-MI, the mice received either 5 × 105/100 µL StemBells or vehicle intravenously. The effects of StemBell treatment on the size and stability of aortic root atherosclerotic plaques and the infarcted heart were determined 28 days post-MI via (immuno)histological analyses. Moreover, monocyte subtypes and lipids in the blood were studied. Results. StemBell treatment resulted in significantly increased cap thickness, decreased intra-plaque macrophage density and increased percentage of intra-plaque anti-inflammatory macrophages and chemokines, without affecting plaque size and serum cholesterol/triglycerides. Furthermore, StemBell treatment significantly increased the percentage of anti-inflammatory macrophages within the infarcted myocardium but did not affect cardiac function nor infarct size. Finally, also the average percentage of anti-inflammatory monocytes in the circulation was increased after StemBell therapy. Discussion. StemBell therapy increased cap thickness and decreased intra-plaque inflammation after MI, indicative of stabilized atherosclerotic plaque. It also induced a shift of circulating monocytes and intra-plaque and intra-cardiac macrophages towards anti-inflammatory phenotypes. Hence, StemBell therapy may be a therapeutic option to prevent atherosclerosis acceleration after MI. Subject LifeMHR - Metabolic Health ResearchELSS - Earth, Life and Social SciencesBiomedical InnovationHealthy LivingAdipose tissue–derived stem cellsAtherosclerosisMesenchymal stromal cellsMyocardial infarctionStemBellsTherapy To reference this document use: http://resolver.tudelft.nl/uuid:57c89c77-7d30-42b0-a5fe-dbc54942d46a DOI https://doi.org/10.1016/j.jcyt.2018.05.006 TNO identifier 824683 Source Cytotherapy, 20 (9), 1143-1154 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.