title: Monocyte chemoattractant protein 1-mediated migration of mesenchymal stem cells is a source of intimal hyperplasia.
abstract: Intimal hyperplasia is considered to be a healing response and is a major cause of vessel narrowing after injury, where migration of vascular progenitor cells contributes to pathological events, including transplant arteriosclerosis.
  
  
  
  In this study, we used a rat aortic-allograft model to identify the predominant cell types associated with transplant arteriosclerosis and to identify factors important in their recruitment into the graft. Transplantation of labeled adventitial tissues allowed us to identify the adventitia as a major source of cells migrating to the intima. RNA microarrays revealed a potential role for monocyte chemoattractant protein 1 (MCP-1), stromal cell-derived factor 1, regulated on activation, normal T cell expressed and secreted, and interferon-inducible protein 10 in the induced vasculopathy. MCP-1 induced migration of adventitial fibroblast cells. CCR2, the receptor for MCP-1, was coexpressed with CD90, CD44, NG2, or sca-1 on mesenchymal stem cells. In vivo experiments using MCP-1-deficient and CCR2-deficient mice confirmed an important role of MCP-1 in the formation of intimal hyperplasia in a mouse model of vascular injury.
  
  
  
  The adventitia is a potentially important cellular source that contributes to intimal hyperplasia, and MCP-1 is a potent chemokine for the recruitment of adventitial vascular progenitor cells to intimal lesions.
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Monika K
authors.initials: MK
authors.lastname: Grudzinska
authors.forename: Ewa
authors.initials: E
authors.lastname: Kurzejamska
authors.forename: Nina
authors.initials: N
authors.lastname: Hagemann
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Bojakowski
authors.forename: Joanna
authors.initials: J
authors.lastname: Soin
authors.forename: Michael H
authors.initials: MH
authors.lastname: Lehmann
authors.forename: Hans
authors.initials: H
authors.lastname: Reinecke
authors.forename: Charles E
authors.initials: CE
authors.lastname: Murry
authors.forename: Cecilia
authors.initials: C
authors.lastname: Soderberg-Naucler
authors.forename: Piotr
authors.initials: P
authors.lastname: Religa
mesh_terms: D000818:Animals; D002465:Cell Movement; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D006965:Hyperplasia / Q000235:genetics / Q000473:pathology; D059630:Mesenchymal Stem Cells / Q000166:cytology* / Q000378:metabolism; D051379:Mice; D023421:Models, Animal; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D058426:Neointima / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D012680:Sensitivity and Specificity; D015398:Signal Transduction; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism; D014184:Transplantation, Homologous; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology*; D057772:Vascular System Injuries / Q000473:pathology / Q000503:physiopathology
chemical_list: D018932:Chemokine CCL2
keywords: adventitia; monocyte chemoattractant protein 1; smooth muscle cells; vascular progenitor