title: Abnormality of RUNX1 signal transduction in psoriatic CD34+ bone marrow cells.
abstract: BACKGROUND
  Although it has been shown that T-cell dysfunction in psoriasis correlates with various endogenous and exogenous stimuli, there are also intensive and complicated genetic background effects indicating that intrinsic abnormalities may play a more predominant role such as in haematopoietic cells, the haematopoietic microenvironment and the development of haematopoietic cells into T cells.
  
  
  OBJECTIVE
  To reveal the activity of haematopoietic stem cells from patients with psoriasis.
  
  
  METHODS
  Bone marrow CD34+ cells were isolated and expression levels were tested by reverse transcriptase-polymerase chain reaction and Western blotting. The binding site for RUNX1 located between SLC9A3R1 and NAT9 and the apoptotic index of CD34+ cells were also investigated.
  
  
  RESULTS
  We found that the expression of RUNX1, SLC9A3R1, HLA-C and PRKCB mRNA and RUNX1 protein was significantly higher in patients with psoriasis than in the controls, and SLC9A3R1 expression showed a significant positive correlation with the Psoriasis Area and Severity Index score. There was no statistical significance for PDCD1 mRNA and PKC-β I protein expression levels between the patients with psoriasis and controls. Mutation of RUNX1 binding sites between SLC9A3R1 and NAT9 was not detected, and the apoptotic index in patients with psoriasis showed no statistical significance compared with the controls.
  
  
  CONCLUSIONS
  Expression of the critical transcription factor RUNX1, which regulates CD34+ cell development and differentiation, was abnormal, and augmentation of these expression levels might induce dysfunction of marrow haematopoietic stem cells and the haematopoietic microenvironment and be involved in the progression of psoriasis.
authors.affiliation: Department of Dermatology, Taiyuan Center Hospital, Affiliated to Shanxi Medical University, 1 Dong San Dao Xiang, Taiyuan 030009, Shanxi Province, China.
authors.forename: G
authors.initials: G
authors.lastname: Yin
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.forename: Y
authors.initials: Y
authors.lastname: Wan
authors.forename: R
authors.initials: R
authors.lastname: Hou
authors.forename: X
authors.initials: X
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: T
authors.initials: T
authors.lastname: Cheng
authors.forename: K
authors.initials: K
authors.lastname: Zhang
mesh_terms: D000328:Adult; D018952:Antigens, CD34 / Q000276:immunology*; D017209:Apoptosis / Q000502:physiology; D001665:Binding Sites / Q000235:genetics; D015153:Blotting, Western; D050676:Core Binding Factor Alpha 2 Subunit / Q000378:metabolism*; D005260:Female; D015236:HLA-C Antigens / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D010750:Phosphoproteins / Q000235:genetics / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D064546:Protein Kinase C beta; D011565:Psoriasis / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017422:Sequence Analysis, DNA; D012720:Severity of Illness Index; D015398:Signal Transduction / Q000502:physiology*; D017923:Sodium-Hydrogen Exchangers / Q000235:genetics / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism* / Q000502:physiology
chemical_list: D018952:Antigens, CD34; D050676:Core Binding Factor Alpha 2 Subunit; D015236:HLA-C Antigens; D010750:Phosphoproteins; D012333:RNA, Messenger; C493728:RUNX1 protein, human; D017923:Sodium-Hydrogen Exchangers; C093376:sodium-hydrogen exchanger regulatory factor; D011493:Protein Kinase C; D064546:Protein Kinase C beta