title: HIMeg-1, a cell line derived from a CML patient, is capable of monocytic and megakaryocytic differentiation.
abstract: We have characterized HIMeg-1, a subclone of the promegakaryoblastic cell line HIMeg, in terms of its capability of proliferation and differentiation when it is exposed to various agents. We observed that phorbol 12-myristate 13-acetate (PMA) arrested HIMeg-1 growth and induced expression of monocytic surface antigens CD11c and CD14, but not the megakaryocytic surface antigen CD14a. In addition, PMA treatment of HIMeg-1 led to rapid activation of mRNA expression of egr-1, a transcription factor involved in regulating differentiation of hematopoietic progenitor cells. On the other hand, treatment of HIMeg-1 with the activated peripheral blood lymphocyte-conditioned medium (PBL-CM) resulted in greatly enhanced incorporation of 3H-thymidine into newly synthesized DNA. This enhanced 3H-thymidine incorporation appears to be specific to HIMeg-1 since the same concentrations of PBL-CM had little effect on the growth of the megakaryoblastic leukemia cell line SAM-1. The PBL-CM-induced DNA synthesis in HIMeg-1 was associated with activation of CD41a and CD41b surface antigen expression and down-regulation of expression of the erythroid marker glycophorin A and the early myeloid surface antigen CD33. HIMeg-1 capable of responding differentially to PMA and PBL-CM by changing its growth rate as well as its differentiation patterns will provide an ideal model to study the underlying mechanism regulating lineage restriction of hematopoietic progenitor cells.
authors.affiliation: Hipple Cancer Research Center, Dayton, OH, USA.
authors.forename: T
authors.initials: T
authors.lastname: Cheng
authors.forename: C L
authors.initials: CL
authors.lastname: Erickson-Miller
authors.forename: C
authors.initials: C
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Cardier
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: J
authors.initials: J
authors.lastname: Dempsey
authors.forename: M
authors.initials: M
authors.lastname: Mogle
authors.forename: E
authors.initials: E
authors.lastname: Barbera
authors.forename: M J
authors.initials: MJ
authors.lastname: Murphy
authors.forename: W
authors.initials: W
authors.lastname: Dai
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D000954:Antigens, Surface / Q000378:metabolism; D015152:Blotting, Northern; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002469:Cell Separation; D003470:Culture Media; D004268:DNA-Binding Proteins / Q000235:genetics; D051766:Early Growth Response Protein 1; D005434:Flow Cytometry; D006801:Humans; D017874:Immediate-Early Proteins; D016167:Integrin alphaXbeta2 / Q000378:metabolism; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D018950:Lipopolysaccharide Receptors; D008213:Lymphocyte Activation; D008533:Megakaryocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology*; D009000:Monocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology*; D012333:RNA, Messenger / Q000378:metabolism; D015682:Retroviridae Proteins, Oncogenic / Q000235:genetics; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014157:Transcription Factors; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000276:immunology / Q000473:pathology
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000954:Antigens, Surface; D003470:Culture Media; D004268:DNA-Binding Proteins; C497325:EGR1 protein, human; D051766:Early Growth Response Protein 1; D017874:Immediate-Early Proteins; D016167:Integrin alphaXbeta2; D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger; D015682:Retroviridae Proteins, Oncogenic; D014157:Transcription Factors; D013755:Tetradecanoylphorbol Acetate