title: Mesoangioblasts, vessel-associated multipotent stem cells, repair the infarcted heart by multiple cellular mechanisms: a comparison with bone marrow progenitors, fibroblasts, and endothelial cells.
abstract: OBJECTIVE
  To test the potential of mesoangioblasts (Mabs) in reducing postischemic injury in comparison with bone marrow progenitor cells (BMPCs), fibroblasts (Fbs), and embryonic stem cell-derived endothelial cells (ECs), and to identify putative cellular protective mechanisms.
  
  
  RESULTS
  Cells were injected percutaneously in the left ventricular (LV) chamber of C57BL/6 mice, 3 to 6 hours after coronary ligation, and detected in the hearts 2 days and 6 weeks later. Echocardiographic examinations were performed at 6 weeks. LV dilation was reduced and LV shortening fraction was improved with Mabs and BMPCs but not with ECs and Fbs. Donor cell colonization of the host myocardium was modest and predominantly in the smooth muscle layer of vessels. Capillary density was higher in the peripheral infarct area and apoptotic cardiomyocytes were fewer with Mabs and BMPCs. Mabs and BMPCs, but not Fbs or ECs, promoted survival of cultured cardiocytes under low-oxygen in culture. This activity was present in Mab-conditioned medium and could be replaced by a combination of basic fibroblast growth factor (bFGF), insulin-like growth factor (IGF)-1, and hepatocyte growth factor (HGF), all of which are produced by these cells. Conditioned medium from Mabs, but not from Fbs, stimulated proliferation of smooth muscle cells in vitro.
  
  
  CONCLUSIONS
  Mabs appear as effective as BMPCs in reducing postinfarction LV dysfunction, likely through production of antiapoptotic and angiogenic factors.
authors.affiliation: Stem Cell Research Institute, Dibit, H. San Raffaele, Milan, Italy.
authors.forename: Daniela
authors.initials: D
authors.lastname: Galli
authors.forename: Anna
authors.initials: A
authors.lastname: Innocenzi
authors.forename: Lidia
authors.initials: L
authors.lastname: Staszewsky
authors.forename: Lucia
authors.initials: L
authors.lastname: Zanetta
authors.forename: Maurilio
authors.initials: M
authors.lastname: Sampaolesi
authors.forename: Antonio
authors.initials: A
authors.lastname: Bai
authors.forename: Elena
authors.initials: E
authors.lastname: Martinoli
authors.forename: Eleonora
authors.initials: E
authors.lastname: Carlo
authors.forename: Giovanna
authors.initials: G
authors.lastname: Balconi
authors.forename: Fabio
authors.initials: F
authors.lastname: Fiordaliso
authors.forename: Stefano
authors.initials: S
authors.lastname: Chimenti
authors.forename: Gabriella
authors.initials: G
authors.lastname: Cusella
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Dejana
authors.forename: Giulio
authors.initials: G
authors.lastname: Cossu
authors.forename: Roberto
authors.initials: R
authors.lastname: Latini
mesh_terms: D000818:Animals; D017209:Apoptosis; D001808:Blood Vessels / Q000166:cytology; D004452:Echocardiography; D004730:Endothelium, Vascular / Q000166:cytology / Q000637:transplantation*; D005347:Fibroblasts / Q000166:cytology / Q000637:transplantation*; D006085:Graft Survival; D006412:Hematopoietic Stem Cells / Q000166:cytology* / Q000502:physiology; D008648:Mesoderm / Q000166:cytology; D051379:Mice; D008810:Mice, Inbred C57BL; D039902:Multipotent Stem Cells / Q000166:cytology* / Q000502:physiology; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000166:cytology; D018919:Neovascularization, Physiologic; D033581:Stem Cell Transplantation; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology