title: Characterization, regulation, and targeting of erythroid progenitors in normal and disordered human erythropoiesis.
abstract: OBJECTIVE
  The erythroid progenitors burst-forming unit-erythroid and colony-forming unit-erythroid have a critical role in erythropoiesis. These cells represent a heterogeneous and poorly characterized population with modifiable self-renewal, proliferation and differentiation capabilities. This review focuses on the current state of erythroid progenitor biology with regard to immunophenotypic identification and regulatory programs. In addition, we will discuss the therapeutic implications of using these erythroid progenitors as pharmacologic targets.
  
  
  RESULTS
  Erythroid progenitors are classically characterized by the appearance of morphologically defined colonies in semisolid cultures. However, these prior systems preclude a more thorough understanding of the composite nature of progenitor populations. Recent studies employing novel flow cytometric and cell-based assays have helped to redefine hematopoiesis, and suggest that erythroid progenitors may arise from different levels of the hematopoietic tree. Moreover, the identification of cell surface marker patterns in human burst-forming unit-erythroid and colony-forming unit-erythroid enhance our ability to perform downstream functional and molecular analyses at the population and single cell level. Advances in these techniques have already revealed novel subpopulations with increased self-renewing capacity, roles for erythroid progenitors in globin gene expression, and insights into pharmacologic mechanisms of glucocorticoids and pomalidomide.
  
  
  CONCLUSIONS
  Immunophenotypic and molecular characterization resolves the diversity of erythroid progenitors, and may ultimately lead to the ability to target these progenitors to ameliorate diseases of dyserythropoiesis.
authors.affiliation: aCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Manhasset bDepartment of Molecular Medicine and Pediatrics, Hofstra Northwell School of Medicine, Hempstead, New York cDepartment of Pediatric Hematology/Oncology, Stanford University School of Medicine, Stanford, California dRed Cell Physiology Laboratory, New York Blood Center, New York, New York, USA.
authors.forename: Brian M
authors.initials: BM
authors.lastname: Dulmovits
authors.forename: Jimmy
authors.initials: J
authors.lastname: Hom
authors.forename: Anupama
authors.initials: A
authors.lastname: Narla
authors.forename: Narla
authors.initials: N
authors.lastname: Mohandas
authors.forename: Lionel
authors.initials: L
authors.lastname: Blanc
mesh_terms: D000740:Anemia / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D015415:Biomarkers; D002454:Cell Differentiation / Q000187:drug effects / Q000235:genetics; D049109:Cell Proliferation / Q000187:drug effects; D000066673:Cell Self Renewal / Q000187:drug effects / Q000235:genetics; D015672:Erythroid Precursor Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*; D004920:Erythropoiesis / Q000187:drug effects / Q000235:genetics; D005938:Glucocorticoids / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology / Q000627:therapeutic use; D016130:Immunophenotyping; D010641:Phenotype; D013792:Thalidomide / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D005938:Glucocorticoids; D007155:Immunologic Factors; D013792:Thalidomide; C467566:pomalidomide