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Cilostazol inhibits the expression of hnRNP A2/B1 and cytokines in human dermal microvascular endothelial cells

1, 2, 3, 4, 5, 6, 7

  1. Department of Dermatology, Yanbian University Hospital, Yanji, China.
  2. Department of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian, China.
  3. Department of Pathology, Yanbian University Hospital, Yanji, China.
  4. Department of Dermatology and Cutaneous Biology Research Center, International St. Mary’s Hospital, Catholic Kwandong University, College of Medicine, Incheon, Korea.
  5. Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
  6. Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
  7. Department of Dermatology and Cutaneous Biology Research Center, International St. Mary’s Hospital, Catholic Kwandong University, College of Medicine, Incheon, Korea. dbang@yuhs.ac

CER10182 Submission on line
2017 Vol.35, N°6 ,Suppl.108 - PI 0060, PF 0066
Full Papers

Rheumatology Article

 

Abstract

OBJECTIVES:
hnRNP A2/B1 has been identified as a target antigen of anti-endothelial cell IgA antibody in patients with Behçet’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.

PMID: 28850024 [PubMed]

Received: 15/12/2016 - Accepted : 08/06/2017 - In Press: 28/08/2017 - Published: 27/11/2017