title: The effect of rhG-CSF on spleen transcriptome in mouse leukopenia model induced by cyclophosphamide.
abstract: BACKGROUND
  RhG-CSF significantly elevates the otherwise reduced numbers of leukocytes following chemotherapy. However, prior work has predominantly focused on the effect of rhG-CSF on the hematopoietic system, and few studies have focused on the immune system.
  
  
  OBJECTIVE
  We aimed to investigate the effect of rhG-CSF on the immune system transcriptome in a mouse leukopenia model that was induced by cyclophosphamide.
  
  
  METHODS
  A cyclophosphamide leukopenia model was established in C57BL/6 mice, which were randomly divided into a normal control group (CK), a cyclophosphamide model group (CY) and a rhG-CSF treatment group (rhG-CSF). After 3 d of rhG-CSF treatment, a mouse gene expression microarray enabled evaluation of changes in the transcriptome in the mouse spleen.
  
  
  RESULTS
  About 3552 differentially expressed genes occurred among the three experimental groups, of which 74.9% (2659) concentrated on three gene expression patterns. Gene ontology and pathway analysis of 2659 differential genes showed that early in treatment when leukocyte counts remained low, rhG-CSF recovered the transcription of genes that were related to DNA damage repair and metabolism of nucleotides and amino acids. By contrast, rhG-CSF inhibited the transcription of genes involved in transendothelial migration and endocytosis, and dampened the transcription of genes associated with cell proliferation as compared with the CY group.
  
  
  CONCLUSIONS
  Our study suggests that rhG-CSF recovered metabolism in immune cells, suppressed in vivo immune defense, and attenuated immune cell proliferation in a cyclophosphamide induced leukopenia model. Use of gene expression microarrays can macroscopically and systematically inform the mechanism of rhG-CSF on immune cells.
authors.affiliation: Department of Cytobiology, Institute of Frontier Medical Sciences, Jilin University , Changchun , China .
authors.forename: He
authors.initials: H
authors.lastname: Guo
authors.forename: Fei
authors.initials: F
authors.lastname: Sun
authors.forename: Wei
authors.initials: W
authors.lastname: Huang
authors.forename: Zhiyi
authors.initials: Z
authors.lastname: Liu
authors.forename: Shuqin
authors.initials: S
authors.lastname: Zhang
authors.forename: Qiuli
authors.initials: Q
authors.lastname: Zhou
authors.forename: Chongyang
authors.initials: C
authors.lastname: Liang
mesh_terms: D000818:Animals; D049109:Cell Proliferation / Q000187:drug effects; D003520:Cyclophosphamide / Q000494:pharmacology*; D004260:DNA Repair / Q000187:drug effects / Q000235:genetics; D005260:Female; D015870:Gene Expression / Q000187:drug effects / Q000235:genetics; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D007962:Leukocytes / Q000187:drug effects; D007970:Leukopenia / Q000139:chemically induced* / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011994:Recombinant Proteins / Q000494:pharmacology*; D013154:Spleen / Q000187:drug effects*; D014158:Transcription, Genetic / Q000187:drug effects / Q000235:genetics; D059467:Transcriptome / Q000187:drug effects* / Q000235:genetics
chemical_list: D011994:Recombinant Proteins; D016179:Granulocyte Colony-Stimulating Factor; D003520:Cyclophosphamide