Age-related changes in monocytes exacerbate neointimal hyperplasia after vascular injury
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Laisel Martinez1, Camilo Gomez1 and Roberto I. Vazquez-Padron1*
1 Department of Surgery and Vascular Biology Institute, University of Miami Miller School of Medicine, Miami, FL, USA
Roberto I. Vazquez-Padron, email:
Keywords: age, monocytes, gene expression, balloon injury, neointimal hyperplasia
Received: March 21, 2015 Accepted: March 31, 2015 Published: April 19, 2015
Neointimal hyperplasia is the leading cause of restenosis after endovascular interventions. It is characterized by the accumulation of myofibroblast-like cells and extracellular matrix in the innermost layer of the wall and is exacerbated by inflammation. Monocytes from either young or aged rats were applied perivascularly to injured vascular walls of young recipient animals. Monocytes from aged rats, but not young donors, increased neointima thickness. Accordingly, the gene expression profiles of CD11b+ monocytes from aged rats showed significant up-regulation of genes involved in cellular adhesion, lipid degradation, cytotoxicity, differentiation, and inflammation. These included cadherin 13 (Cdh13), colony stimulating factor 1 (Csf1), chemokine C-X-C motif ligand 1 (Cxcl1), endothelial cell-selective adhesion molecule (Esam), and interferon gamma (Ifng). In conclusion, our results suggest that the increased inflammatory and adhesive profile of monocytes contributes to pathological wall remodeling in aged-related vascular diseases.
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