PMID- 20195728
OWN - NLM
STAT- MEDLINE
DCOM- 20101122
LR  - 20211020
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 33
IP  - 5
DP  - 2010 Oct
TI  - Prostaglandin I(2) analogues enhance growth-related oncogene-alpha expression in 
      human monocyte-derived dendritic cells.
PG  - 334-43
LID - 10.1007/s10753-010-9190-7 [doi]
AB  - Chemokines for neutrophils such as growth-related oncogene-alpha (GRO-alpha) are 
      important in patients with refractory or severe asthma. Prostaglandin I(2) 
      (PGI(2)) analogues were regarded as potential treatments for asthma. Dendritic 
      cells (DCs) are the professional antigen-presenting cells and play a critical 
      role in regulating immune response. However, it is unknown whether PGI(2) 
      analogues have regulatory effects on GRO-alpha expression in human 
      monocyte-derived DCs (MDDCs). The human MDDCs were pretreated with iloprost and 
      treprostinil (two PGI(2) analogues) or forskolin, a cyclic adenosine 
      monophosphate (cAMP) activator, before stimulation with lipopolysaccharide (LPS). 
      In some cases, I prostanoid (IP) receptor and E prostanoid (EP) antagonists were 
      pretreated before PGI(2) analogue treatment. To investigate the intracellular 
      signaling, nuclear factor (NF)-kappaB inhibitor and the mitogen-activated protein 
      kinase (MAPK) inhibitors were pretreated before PGI(2) analogue treatment. 
      GRO-alpha was measured by enzyme-linked immunosorbent assay. Intracellular 
      signaling was also investigated by Western blot. Iloprost and treprostinil 
      enhanced LPS-induced GRO-alpha expression in MDDCs. This effect could be reversed 
      by an I prostanoid receptor antagonist, CAY10449, but not EP receptor 
      antagonists. Forskolin conferred a similar modulating effect as that noted in 
      iloprost- and treprostinil-treated MDDCs. PGI(2) analogue-enhanced LPS-induced 
      GRO-alpha expression was reduced by MAPK-p38 inhibitor, SB203580. PGI(2) 
      analogues enhanced LPS-induced phospho-p38 expression. PGI(2) analogues enhanced 
      LPS-induced GRO-alpha expression via the IP receptor-cAMP and p38-MAPK pathways 
      in human MDDCs, which may further recruit neutrophil accumulation and adversely 
      affect patients with refractory or severe asthma because of airway neutrophilia. 
      These effects should be considered for PGI(2) analogues as candidates for the 
      treatment of asthma.
FAU - Kuo, Chang-Hung
AU  - Kuo CH
AD  - Department of Pediatrics, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, 
      Taiwan, Republic of China.
FAU - Jan, Ren-Long
AU  - Jan RL
FAU - Chu, Yu-Te
AU  - Chu YT
FAU - Wang, Wei-Li
AU  - Wang WL
FAU - Huang, Ming-Yii
AU  - Huang MY
FAU - Huang, Ching-Hua
AU  - Huang CH
FAU - Chen, Tai-Heng
AU  - Chen TH
FAU - Hung, Chih-Hsing
AU  - Hung CH
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Anti-Asthmatic Agents)
RN  - 0 (CXCL1 protein, human)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Enzyme Activators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (PTGIR protein, human)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Receptors, Epoprostenol)
RN  - 0 (Receptors, Prostaglandin)
RN  - 0 (Receptors, Prostaglandin E)
RN  - DCR9Z582X0 (Epoprostenol)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - JED5K35YGL (Iloprost)
RN  - RUM6K67ESG (treprostinil)
SB  - IM
MH  - Anti-Asthmatic Agents/*pharmacology
MH  - Blotting, Western
MH  - Case-Control Studies
MH  - Cells, Cultured
MH  - Chemokine CXCL1/*metabolism
MH  - Cyclic AMP/metabolism
MH  - Dendritic Cells/*drug effects/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Enzyme Activators/pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Epoprostenol/*analogs & derivatives/*pharmacology
MH  - Humans
MH  - Iloprost/*pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism
MH  - NF-kappa B/antagonists & inhibitors/metabolism
MH  - Phosphorylation
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Receptors, Epoprostenol
MH  - Receptors, Prostaglandin/antagonists & inhibitors/metabolism
MH  - Receptors, Prostaglandin E/antagonists & inhibitors/metabolism
MH  - Signal Transduction/drug effects
MH  - Up-Regulation
EDAT- 2010/03/03 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/03/03 06:00
PHST- 2010/03/03 06:00 [entrez]
PHST- 2010/03/03 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
AID - 10.1007/s10753-010-9190-7 [doi]
PST - ppublish
SO  - Inflammation. 2010 Oct;33(5):334-43. doi: 10.1007/s10753-010-9190-7.