title: Evaluation of H3 histone methylation and colony formation in erythroid progenitors treated with thalidomide and sodium butyrate.
abstract: OBJECTIVE
  β-thalassemia and sickle cell disease are hemoglobinopathies with reduced/absent β chains in the former and dysfunctional β chains in the latter. In both conditions, up-regulation of hemoglobin F through demethylation can alleviate the symptoms. This can be attained with drugs such as thalidomide and sodium butyrate.
  
  
  METHODS
  This study was performed on erythroid progenitors derived from CD133+ cord blood stem cells. Erythroid progenitors were treated with thalidomide and sodium butyrate in single and combined groups. Colony-formation potential in each group was evaluated by the colony assay. Real-time polymerase chain reaction (RT-PCR) was used to evaluate the effect of these drugs on histone H3 lysine 27 (H3K27) methylation patterns.
  
  
  RESULTS
  Compared to other treatment groups, CD133+ cells treated with thalidomide alone produced more hematopoietic colonies. Thalidomide alone was also more effective in decreasing H3K27 methylation.
  
  
  CONCLUSIONS
  Thalidomide shows superiority to sodium butyrate as a hypomethylating agent in this cell culture study, and it has the potential to become conventional treatment for sickle cell disease and β-thalassemia.
authors.affiliation: Department of Hematology and Blood Banking, Tarbiat Modares University, Tehran, Iran.
authors.forename: Ali Dehghani
authors.initials: AD
authors.lastname: Fard
authors.forename: Saeid
authors.initials: S
authors.lastname: Kaviani
authors.forename: Mehrdad
authors.initials: M
authors.lastname: Noruzinia
authors.forename: Masoud
authors.initials: M
authors.lastname: Soleimani
authors.forename: Saeid
authors.initials: S
authors.lastname: Abroun
authors.forename: Rouzbeh
authors.initials: R
authors.lastname: Chegeni
authors.forename: Abbas
authors.initials: A
authors.lastname: Hajifathali
authors.forename: Zahra
authors.initials: Z
authors.lastname: Zonoubi
authors.forename: Mohammad
authors.initials: M
authors.lastname: Ahmadvand
authors.forename: Majid Mossahebi
authors.initials: MM
authors.lastname: Mohammadi
authors.forename: Najmaldin
authors.initials: N
authors.lastname: Saki
mesh_terms: D000071916:AC133 Antigen; D000755:Anemia, Sickle Cell / Q000188:drug therapy / Q000378:metabolism; D015703:Antigens, CD; D002087:Butyrates / Q000494:pharmacology*; D002478:Cells, Cultured; D015672:Erythroid Precursor Cells / Q000378:metabolism*; D005312:Fetal Blood; D005319:Fetal Hemoglobin / Q000096:biosynthesis; D006023:Glycoproteins; D006657:Histones / Q000378:metabolism*; D006801:Humans; D008745:Methylation / Q000187:drug effects; D010455:Peptides; D060888:Real-Time Polymerase Chain Reaction; D013723:Teratogens / Q000494:pharmacology*; D013792:Thalidomide / Q000494:pharmacology*; D015854:Up-Regulation / Q000187:drug effects; D017086:beta-Thalassemia / Q000188:drug therapy / Q000378:metabolism
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D002087:Butyrates; D006023:Glycoproteins; D006657:Histones; C000606023:PROM1 protein, human; D010455:Peptides; D013723:Teratogens; D013792:Thalidomide; D005319:Fetal Hemoglobin