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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Curr+Opin+Hematol
2017 ; 24
(3
): 159-166
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Characterization, regulation, and targeting of erythroid progenitors in normal
and disordered human erythropoiesis
#MMPMID28099275
Dulmovits BM
; Hom J
; Narla A
; Mohandas N
; Blanc L
Curr Opin Hematol
2017[May]; 24
(3
): 159-166
PMID28099275
show ga
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.