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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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StemBell therapy stabilizes atherosclerotic plaques after myocardial infarction
Linde Woudstra1, Elisa Meinster2, Laura VAN Haren2
1Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands,; ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands,.
Cytotherapy
|August 16, 2018
Summary
StemBell therapy, using adipose stem cells coupled to microbubbles, stabilized atherosclerotic plaques after myocardial infarction by increasing cap thickness and reducing inflammation. This approach may prevent atherosclerosis progression post-MI.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Immunology
Background:
- Atherosclerosis accelerates post-myocardial infarction (MI), destabilizing plaques.
- Mesenchymal stromal cells show therapeutic potential for atherosclerosis.
- StemBells (adipose stem cells coupled to microbubbles) offer a novel delivery method for stem cell therapy post-MI.
Purpose of the Study:
- To investigate the effect of StemBell therapy on atherosclerotic plaque size and stability in a mouse model after MI.
- To assess the impact of StemBell therapy on cardiac tissue and circulating immune cells post-MI.
Main Methods:
- Atherosclerotic mice (Apolipoprotein E-deficient) were subjected to MI and subsequently treated with StemBells or vehicle.
- Aortic root plaques and infarcted hearts were analyzed using (immuno)histological methods 28 days post-MI.
- Monocyte subtypes and serum lipids were quantified.
Main Results:
- StemBell therapy increased atherosclerotic plaque cap thickness and reduced intra-plaque macrophage density.
- A significant increase in anti-inflammatory macrophages and chemokines within plaques and myocardium was observed.
- Circulating monocytes and intra-plaque macrophages shifted towards anti-inflammatory phenotypes, without affecting plaque size or cardiac function.
Conclusions:
- StemBell therapy demonstrates potential for stabilizing atherosclerotic plaques after MI by reducing inflammation and promoting anti-inflammatory responses.
- The therapy induces a favorable shift in immune cell phenotypes, suggesting a strategy to prevent post-MI atherosclerosis acceleration.
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