title: Human cardiac mesoangioblasts isolated from hypertrophic cardiomyopathies are greatly reduced in proliferation and differentiation potency.
abstract: OBJECTIVE
  Our objective was to test whether progenitor cell proliferation and differentiation potential may vary depending upon the disease of the donor.
  
  
  RESULTS
  Human cardiac mesoangioblasts were isolated from cardiac muscle biopsies of patients undergoing open heart surgery for correction of mitral regurgitation following an acute myocardial infarction (MR-MI) or correction of mitral and aortic regurgitation with ensuing left ventricular hypertrophy (MAR-LVH). The cells express surface markers and cardiac genes similar to mouse cardiac mesoangioblasts; they have limited self-renewing and clonogenic activity and are committed mainly to cardiogenesis. Although cardiac differentiation can be induced by 5-azacytidine or by co-culture with rat neonatal cardiomyocytes, human cells do not contract spontaneously like their mouse counterparts. When locally injected in the infarcted myocardium of immunodeficient mice, cardiac mesoangioblasts generate a chimeric heart that contains human myocytes and some capillaries; likewise, they colonize chick embryo hearts when transplanted in ovo. At variance with cells from patients with MR-MI, when isolation was performed on biopsies from MAR-LVH, cells could be isolated in much lower numbers, proliferated less extensively and failed to differentiate.
  
  
  CONCLUSIONS
  Cardiac mesoangioblasts are present in the human heart but this endogenous progenitor population is progressively exhausted, possibly by continuous and inefficient regeneration attempts.
authors.affiliation: Division of Regenerative Medicine, San Raffaele Scientific Institute, 58 Via Olgettina, 20132 Milan, Italy. bggalvez@hotmail.com
authors.forename: Beatriz G
authors.initials: BG
authors.lastname: Gálvez
authors.forename: Diego
authors.initials: D
authors.lastname: Covarello
authors.forename: Rosanna
authors.initials: R
authors.lastname: Tolorenzi
authors.forename: Silvia
authors.initials: S
authors.lastname: Brunelli
authors.forename: Arianna
authors.initials: A
authors.lastname: Dellavalle
authors.forename: Stefania
authors.initials: S
authors.lastname: Crippa
authors.forename: Salman Afroze Azmi
authors.initials: SA
authors.lastname: Mohammed
authors.forename: Ludovica
authors.initials: L
authors.lastname: Scialla
authors.forename: Ivan
authors.initials: I
authors.lastname: Cuccovillo
authors.forename: Fabiola
authors.initials: F
authors.lastname: Molla
authors.forename: Lidia
authors.initials: L
authors.lastname: Staszewsky
authors.forename: Francesco
authors.initials: F
authors.lastname: Maisano
authors.forename: Maurilio
authors.initials: M
authors.lastname: Sampaolesi
authors.forename: Roberto
authors.initials: R
authors.lastname: Latini
authors.forename: Giulio
authors.initials: G
authors.lastname: Cossu
mesh_terms: D053687:Adult Stem Cells / Q000473:pathology* / Q000637:transplantation; D000818:Animals; D001022:Aortic Valve Insufficiency / Q000473:pathology; D002312:Cardiomyopathy, Hypertrophic / Q000473:pathology*; D002454:Cell Differentiation; D049109:Cell Proliferation; D002469:Cell Separation; D002478:Cells, Cultured; D002642:Chick Embryo; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D016513:Mice, SCID; D008944:Mitral Valve Insufficiency / Q000473:pathology; D009203:Myocardial Infarction / Q000473:pathology / Q000628:therapy; D009206:Myocardium / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000473:pathology; D051381:Rats; D033581:Stem Cell Transplantation