PMID- 25490414
OWN - NLM
STAT- MEDLINE
DCOM- 20150724
LR  - 20171116
IS  - 1533-4023 (Electronic)
IS  - 0160-2446 (Linking)
VI  - 64
IP  - 6
DP  - 2014 Dec
TI  - Statin inhibits the expression of secretory phospholipase A2 and subsequent 
      monocyte chemoattractant protein-1 in human endothelial cells.
PG  - 489-96
LID - 10.1097/FJC.0000000000000147 [doi]
AB  - Phospholipase A2 (PLA2) changes the phosphatidylcholine contained in low-density 
      lipoprotein (LDL) to lysophosphatidylcholine (LPC), which has various 
      proatherogenic properties. We reported that tumor necrosis factor-alpha (TNFalpha) 
      enhanced the expression of group V PLA2 (sPLA2-V) in human umbilical vein 
      endothelial cells (HUVECs), and the LPC content in LDL and the monocyte 
      chemoattractant protein-1 (MCP-1) expression were augmented when TNFalpha-stimulated 
      HUVECs were incubated with LDL. Here, we observed that an HMG-CoA reductase 
      inhibitor, pitavastatin, at the concentration of >1 muM administered 12 hours 
      before TNFalpha stimulation suppressed the enhancement of sPLA2-V mRNA and protein. 
      Pitavastatin also prevented the enhancement of the LPC content in LDL and the 
      expression of MCP-1 mRNA when TNFalpha-stimulated HUVECs were incubated with LDL. The 
      administration of geranylgeranyl pyrophosphate restored the expression of sPLA2-V 
      mRNA and protein. The administration of the Rho kinase inhibitor Y-27632 and the 
      transfection of small interfering RNA (siRNA) against sPLA2-V before TNFalpha 
      stimulation both diminished the TNFalpha-induced sPLA2-V mRNA expression. Therefore, 
      Y-27632 and siRNA against sPLA2-V also prevented the enhancement of MCP-1 mRNA 
      expression when TNFalpha-stimulated HUVECs were incubated with LDL. Pitavastatin's 
      inhibitory effect on the expression of sPLA2-V induced by TNFalpha may be useful to 
      prevent the proatherogenic modification of LDL.
FAU - Sonoki, Kazuo
AU  - Sonoki K
AD  - *Department of Oral Health Management, School of Oral Health Sciences, Kyushu 
      Dental University, Kitakyushu, Japan; daggerDiabetes Center, Hakujyuji Hospital, 
      Fukuoka, Japan; double daggerDepartment of Medicine and Clinical Science, Graduate School of 
      Medical Sciences, Kyushu University, Fukuoka, Japan;  section signDepartment of Clinical 
      Pharmacokinetics, Graduate School of Pharmaceutical Sciences, Kyushu University, 
      Fukuoka, Japan; and  paragraph signDivision of General Internal Medicine, Department of Health 
      Promotion, Science of Health Improvement, Kyushu Dental University, Kitakyushu, 
      Japan.
FAU - Iwase, Masanori
AU  - Iwase M
FAU - Ohdo, Shigehiro
AU  - Ohdo S
FAU - Ieiri, Ichiro
AU  - Ieiri I
FAU - Takata, Yutaka
AU  - Takata Y
FAU - Kitazono, Takanari
AU  - Kitazono T
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Amides)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Lysophosphatidylcholines)
RN  - 0 (Polyisoprenyl Phosphates)
RN  - 0 (Pyridines)
RN  - 0 (Quinolines)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 138381-45-0 (Y 27632)
RN  - EC 3.1.1.4 (Phospholipases A2, Secretory)
RN  - M5681Q5F9P (pitavastatin)
RN  - N21T0D88LX (geranylgeranyl pyrophosphate)
SB  - IM
MH  - Amides/pharmacology
MH  - Chemokine CCL2/*genetics
MH  - Human Umbilical Vein Endothelial Cells/drug effects/metabolism
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/administration & 
      dosage/*pharmacology
MH  - Lipoproteins, LDL/metabolism
MH  - Lysophosphatidylcholines/metabolism
MH  - Phospholipases A2, Secretory/*genetics
MH  - Polyisoprenyl Phosphates/pharmacology
MH  - Pyridines/pharmacology
MH  - Quinolines/administration & dosage/*pharmacology
MH  - RNA, Messenger/metabolism
MH  - RNA, Small Interfering/administration & dosage
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2014/12/10 06:00
MHDA- 2015/07/25 06:00
CRDT- 2014/12/10 06:00
PHST- 2014/12/10 06:00 [entrez]
PHST- 2014/12/10 06:00 [pubmed]
PHST- 2015/07/25 06:00 [medline]
AID - 00005344-201412000-00001 [pii]
AID - 10.1097/FJC.0000000000000147 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 2014 Dec;64(6):489-96. doi: 10.1097/FJC.0000000000000147.