PMID- 24337644
OWN - NLM
STAT- MEDLINE
DCOM- 20140918
LR  - 20131223
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 33
IP  - 2
DP  - 2014 Feb
TI  - The 15-deoxy-delta12,14-prostaglandin J2 inhibits LPS‑stimulated inflammation via 
      enhancement of the platelet‑activating factor acetylhydrolase activity in human 
      retinal pigment epithelial cells.
PG  - 449-56
LID - 10.3892/ijmm.2013.1588 [doi]
AB  - A well-recognized natural ligand of PPARgamma, 15-deoxy-delta(12,14)-prostaglandin J(2) 
      (15d-PGJ(2)) possesses immunomodulatory properties. The aim of this study was to 
      elucidate whether 15d-PGJ(2) was able to attenuate lipopolysaccharide 
      (LPS)-induced inflammatory responses in human retinal pigment epithelial (RPE) 
      cells, which are involved in ocular immune responses. In addition, we examined 
      whether the platelet activating factor (PAF) is associated with the 
      anti-inflammatory activity of 15d-PGJ(2). ARPE19 cells treated with varying 
      concentrations of 15d-PGJ(2) and a PAF antagonist (CV3988) were used in this 
      study. The activity of PAF-acetylhydrolase (PAF-AH) was assayed by treatment with 
      15d-PGJ(2) and CV3988 in the presence of LPS. 15d-PGJ(2) and CV3988 inhibited the 
      LPS-induced mRNA expression and protein production of interleukin-6 (IL-6), 
      monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule-1 
      (ICAM-1) in ARPE19 cells. These effects resulting from 15d-PGJ(2) were not 
      abrogated by the PPARgamma antagonist, indicating that the actions were 
      PPARgamma-independent. Furthermore, 15d-PGJ(2) and CV3988 enhanced the PAF-AH 
      activity. Additionally, 15d-PGJ(2) inhibited the phosphorylation of the 
      extracellular signal-regulated kinase (ERK) and the activation of nuclear 
      transcription factor-kappaB (NF-kappaB). These results demonstrated that 15d-PGJ(2) 
      reduced LPS-stimulated inflammatory responses in ARPE19 cells by enhancing the 
      PAH-AH activity. These results suggest that 15d-PGJ(2) may have potent 
      anti-inflammatory activity against ocular inflammation.
FAU - Jung, Won-Kyo
AU  - Jung WK
AD  - Department of Biomedical Engineering, Pukyong National University, Busan, 
      Republic of Korea.
FAU - Lee, Chang-Min
AU  - Lee CM
AD  - Department of Microbiology and Immunology, Medical Research Institute, Pusan 
      National University School of Medicine, Yang-san, Republic of Korea.
FAU - Lee, Dae-Sung
AU  - Lee DS
AD  - POSTECH Ocean Science and Technology Institute, Pohang University of Science and 
      Technology, Pohang, Republic of Korea.
FAU - Na, Giyoun
AU  - Na G
AD  - Department of Microbiology, College of Medicine Inje University, Busan, Republic 
      of Korea.
FAU - Lee, Da-Young
AU  - Lee DY
AD  - Department of Microbiology, College of Medicine Inje University, Busan, Republic 
      of Korea.
FAU - Choi, Inhak
AU  - Choi I
AD  - Department of Microbiology, College of Medicine Inje University, Busan, Republic 
      of Korea.
FAU - Park, Sae-Gwang
AU  - Park SG
AD  - Department of Microbiology, College of Medicine Inje University, Busan, Republic 
      of Korea.
FAU - Seo, Su-Kil
AU  - Seo SK
AD  - Department of Microbiology, College of Medicine Inje University, Busan, Republic 
      of Korea.
FAU - Yang, Jae-Wook
AU  - Yang JW
AD  - Department of Ophthalmology, Busan Paik Hospital, College of Medicine Inje 
      University, Busan, Republic of Korea.
FAU - Choi, Jung Sik
AU  - Choi JS
AD  - Department of Internal Medicine, Busan Paik Hospital, College of Medicine Inje 
      University, Busan, Republic of Korea.
FAU - Lee, Young-Min
AU  - Lee YM
AD  - Department of Internal Medicine, Busan Paik Hospital, College of Medicine Inje 
      University, Busan, Republic of Korea.
FAU - Park, Won Sun
AU  - Park WS
AD  - Institute of Medical Sciences, Department of Physiology, Kangwon National 
      University School of Medicine, Chuncheon, Republic of Korea.
FAU - Choi, Il-Whan
AU  - Choi IW
AD  - Department of Microbiology, College of Medicine Inje University, Busan, Republic 
      of Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131213
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (15-deoxy-delta(12,14)-prostaglandin J2)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (PPAR gamma)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 3.1.1.47 (1-Alkyl-2-acetylglycerophosphocholine Esterase)
RN  - RXY07S6CZ2 (Prostaglandin D2)
SB  - IM
MH  - 1-Alkyl-2-acetylglycerophosphocholine Esterase/*metabolism
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cell Survival/drug effects
MH  - Chemokine CCL2/antagonists & inhibitors/genetics/metabolism
MH  - Epithelial Cells/*enzymology
MH  - Extracellular Signal-Regulated MAP Kinases/antagonists & 
      inhibitors/genetics/metabolism
MH  - Humans
MH  - Inflammation/chemically induced/*metabolism
MH  - Intercellular Adhesion Molecule-1/genetics/metabolism
MH  - Interleukin-6/antagonists & inhibitors/genetics/metabolism
MH  - Lipopolysaccharides
MH  - NF-kappa B/antagonists & inhibitors/genetics/metabolism
MH  - PPAR gamma/antagonists & inhibitors/genetics/metabolism
MH  - Phosphorylation
MH  - Prostaglandin D2/*analogs & derivatives/pharmacology
MH  - Retinal Pigment Epithelium/cytology
EDAT- 2013/12/18 06:00
MHDA- 2014/09/19 06:00
CRDT- 2013/12/17 06:00
PHST- 2013/08/30 00:00 [received]
PHST- 2013/12/11 00:00 [accepted]
PHST- 2013/12/17 06:00 [entrez]
PHST- 2013/12/18 06:00 [pubmed]
PHST- 2014/09/19 06:00 [medline]
AID - 10.3892/ijmm.2013.1588 [doi]
PST - ppublish
SO  - Int J Mol Med. 2014 Feb;33(2):449-56. doi: 10.3892/ijmm.2013.1588. Epub 2013 Dec 
      13.