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Cilostazol inhibits the expression of hnRNP A2/B1 and cytokines in human dermal microvascular endothelial cells
Y. An1, Z. Zheng2, X. Zhang3, S.B. Cho4, D.Y. Kim5, M.J. Choi6, D. Bang7
- Department of Dermatology, Yanbian University Hospital, Yanji, China.
- Department of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian, China.
- Department of Pathology, Yanbian University Hospital, Yanji, China.
- Department of Dermatology and Cutaneous Biology Research Center, International St. Mary’s Hospital, Catholic Kwandong University, College of Medicine, Incheon, Korea.
- Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
- Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
- 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
2017 Vol.35, N°6 ,Suppl.108
PI 0060, PF 0066
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PMID: 28850024 [PubMed]
Received: 15/12/2016
Accepted : 08/06/2017
In Press: 28/08/2017
Published: 27/11/2017
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.
