Cardiovascular Research Advance Access originally published online on October 7, 2007
Cardiovascular Research 2008 77(3):471-480; doi:10.1093/cvr/cvm034
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Role of human smooth muscle cell progenitors in atherosclerotic plaque development and composition
1 INSERM U689, Hôpital Lariboisière, 41, Bd de la Chapelle, 75010 Paris, France
2 INSERM U589, Institut L. Bugnard,CHU Rangueil, 31403 Toulouse, France
3 Service de Cardiologie, Hôpital Lariboisière, Paris, France
4 Institut des Vaisseaux et du Sang, Hopital Lariboisiere, Paris, France
* Corresponding author. Tel: +33 1 53216695; fax: +33 1 42813128. E-mail address: tedgui{at}larib.inserm.fr
Aims: We analysed the possible protective role of human endothelial (EPCs) and smooth muscle (SPCs) progenitor cells on atherosclerosis development in apoE–/–RAG2–/– mice. We determined plasma levels of SPCs in coronary patients.
Methods and results: ApoE–/–RAG2–/– mice received four intravenous injections of saline, 5 x 105 SPCs, or 5 x 105 EPCs every other week, one (preventive approach) or 12(curative approach) weeks after starting a high fat diet. Derived-SPC levels were quantified from blood mononuclear cells of patients with stable angina (n = 10) and acute coronary syndromes (ACS, n = 9). SPCs reduced atherosclerosis development by 42% (P < 0.001), but had no effect on lesion progression. In the SPC group, collagen and smooth muscle cell content were increased (+80%, P < 0.001, +46%, P < 0.05, respectively), and macrophage content was decreased (–41%, P < 0.05). In the curative approach, macrophage content decreased by 40.5% (P < 0.05) after SPC injection. EPC injection had no effect on atherosclerosis development or progression. Peripheral blood-derived SPC levels were reduced in patients with ACS compared with stable angina patients (P < 0.05).
Conclusion: We demonstrate that SPCs limit plaque development and promote changes in plaque composition towards a stable phenotype in mice. Our finding in patients suggests that reduced peripheral blood-derived SPC levels might represent a mechanism contributing to plaque destabilization.
KEYWORDS Vascular progenitor cells; Cell therapy; Atherosclerosis; Coronary syndrome
Time for primary review: 18 days
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