title: Dissecting the molecular relationship among various cardiogenic progenitor cells.
abstract: BACKGROUND
  Multiple progenitors derived from the heart and bone marrow (BM) have been used for cardiac repair. Despite this, not much is known about the molecular identity and relationship among these progenitors. To develop a robust stem cell therapy for the heart, it is critical to understand the molecular identity of the multiple cardiogenic progenitor cells.
  
  
  OBJECTIVE
  This study is the first report of high-throughput transcriptional profiling of cardiogenic progenitor cells carried out on an identical platform.
  
  
  RESULTS
  Microarray-based transcriptional profiling was carried out for 3 cardiac (ckit(+), Sca1(+), and side population) and 2 BM (ckit(+) and mesenchymal stem cell) progenitors, obtained from age- and sex-matched wild-type C57BL/6 mice. Analysis indicated that cardiac-derived ckit(+) population was very distinct from Sca1(+) and side population cells in the downregulation of genes encoding for cell-cell and cell-matrix adhesion proteins, and in the upregulation of developmental genes. Significant enrichment of transcripts involved in DNA replication and repair was observed in BM-derived progenitors. The BM ckit(+) cells seemed to have the least correlation with the other progenitors, with enrichment of immature neutrophil-specific molecules.
  
  
  CONCLUSIONS
  Our study indicates that cardiac ckit(+) cells represent the most primitive population in the rodent heart. Primitive cells of cardiac versus BM origin differ significantly with respect to stemness and cardiac lineage-specific genes, and molecules involved in DNA replication and repair. The detailed molecular profile of progenitors reported here will serve as a useful reference to determine the molecular identity of progenitors used in future preclinical and clinical studies.
authors: Division of Cardiology, Department of Medicine, Stanford Cardiovascular Institute, Institute of Stem Cell Biology & Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305-5454, USA.
authors: Devaveena
authors: D
authors: Dey
authors: Leng
authors: L
authors: Han
authors: Michael
authors: M
authors: Bauer
authors: Fumihiro
authors: F
authors: Sanada
authors: Angelos
authors: A
authors: Oikonomopoulos
authors: Toru
authors: T
authors: Hosoda
authors: Kazumasa
authors: K
authors: Unno
authors: Patricia
authors: P
authors: De Almeida
authors: Annarosa
authors: A
authors: Leri
authors: Joseph C
authors: JC
authors: Wu
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D001854:Bone Marrow Cells / Q000378:metabolism*; D002448:Cell Adhesion / Q000235:genetics; D002450:Cell Communication / Q000235:genetics; D002454:Cell Differentiation / Q000235:genetics; D019070:Cell Lineage / Q000235:genetics; D002478:Cells, Cultured; D004260:DNA Repair / Q000235:genetics; D004261:DNA Replication / Q000235:genetics; D005434:Flow Cytometry; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental; D057166:High-Throughput Screening Assays; D018189:Immunomagnetic Separation; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D059630:Mesenchymal Stem Cells / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D032383:Myocytes, Cardiac / Q000378:metabolism*; D010641:Phenotype; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics; D013234:Stem Cells / Q000378:metabolism*
chemical_list: D000950:Antigens, Ly; D015415:Biomarkers; C074650:Ly6a protein, mouse; D008565:Membrane Proteins; D012333:RNA, Messenger; D019009:Proto-Oncogene Proteins c-kit