TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000508487
  • Gene Name:CXCL2
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:qPCR
  • mRNA Pathway:NA
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB01166
  • Drug Name:Cilostazol
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:bipolar disorder
  • Tissue:patients tissues

Other information

  • Title:Cilostazol inhibits the expression of hnRNP A2/B1 and cytokines in human dermal microvascular endothelial cells
  • Journal:Clinical And Experimental Rheumatology
  • Published:2017
  • PubMed ID:28850024
  • Abstract:Objectives:hnRNP A2/B1 has been identified as a target antigen of anti-endothelial cell IgA antibody in patients with Beh?et＇s disease (BD). In addition, increased expression of cellular hnRNP A2/B1 is stimulated by Streptococcus sanguinis or the sera from patients with BD. We aimed to investigate the effects of cilostazol on the expression of hnRNP A2/B1 and chemokines in human dermal microvascular endothelial cells (HDMECs). Methods:Expression of hnRNP A2/B1, cytokines, and chemokines in HDMECs was induced by tumour necrosis factor (TNF)-α, interleukin (IL)-1β, and lipopolysaccharide (LPS). HDMECs were treated with cilostazol (10 μM) and the inhibitory effects were evaluated with real-time polymerase chain reaction and immunocytochemistry. Results:Expression of hnRNP A2/B1, CXCL1, CXCL2, CXCL8, and IL-1β mRNA was significantly increased in HDMECs treated with all three stimulants. In addition, mRNA expression of hnRNP A2/B1 and inflammatory mediators was significantly inhibited in HDMECs treated with various stimulants with cilostazol pretreatment. Immunocytochemistry demonstrated that cilostazol pretreatment effectively inhibited the stimulant-induced increased expression of hnRNP A2/B1 in the nucleus and cytoplasm of HDMECs. Conclusions:Cilostazol pretreatment can reduce the excessive expression of inflammatory cytokines and chemokines and hnRNP A2/B1 by the BD-related stimulants, including TNF-α, IL-1β, and LPS, in HDMECs. We suggest that cilostazol may have therapeutic efficacy in inhibiting the major inflammatory reaction in the pathogenesis of BD.
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