PMID- 12647268
OWN - NLM
STAT- MEDLINE
DCOM- 20030425
LR  - 20161124
IS  - 0026-0495 (Print)
IS  - 0026-0495 (Linking)
VI  - 52
IP  - 3
DP  - 2003 Mar
TI  - Atherogenic role of lysophosphatidylcholine in low-density lipoprotein modified 
      by phospholipase A2 and in diabetic patients: protection by nitric oxide donor.
PG  - 308-14
AB  - The aim of our study was to investigate the atherogenic role of 
      lysophosphatidylcholine (lyso-PC) in low-density lipoprotein (LDL) under diabetic 
      environment. Expression of monocyte chemoattractant protein-1 (MCP-1) mRNA and 
      nuclear factor-kappa B (NF-kappaB)-DNA binding activity were determined in human 
      umbilical vein endothelial cells (HUVEC) incubated with native or glycoxidized 
      LDL, LDL modified by phospholipase A2 (PLA2) and LDL isolated from diabetic 
      patients. Lyso-PC contents in LDL were measured using electrospray 
      ionization-liquid chromatography/mass spectrometry (ESI-LC/MS). Lyso-PC contents 
      were higher in glycoxidized LDL and PLA2-treated LDL compared with native LDL. 
      Glycoxidized LDL and enrichment of lyso-PC by PLA2 treatment resulted in 
      upregulation of MCP-1 mRNA expression through increased NF-kappaB activity in 
      HUVEC. Moreover, LDL isolated from diabetics contained more lyso-PC than that 
      from nondiabetic subjects, and induced higher MCP-1 mRNA expression and NF-kappaB 
      activity in HUVEC. In both in vitro and human studies, palmitoyl- and 
      stearoyl-lyso-PC contents correlated with MCP-1 expression and NF-kappaB 
      activity. Preincubation with 4-ethyl-2-hydroxyimino-5-nitro-3-hexenamide, a NO 
      donor, abrogated increased expression of MCP-1 mRNA and high NF-kappaB activity 
      induced by PLA2-treated LDL and by LDL isolated from diabetic patients. Our 
      results suggest that lyso-PC contents in LDL play an important role in 
      atherogenesis under diabetic condition, which could be prevented by increased 
      availability of vascular NO.
CI  - Copyright 2003, Elsevier Science (USA). All rights reserved.
FAU - Sonoki, Kazuo
AU  - Sonoki K
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Iwase, Masanori
AU  - Iwase M
FAU - Iino, Kenzo
AU  - Iino K
FAU - Ichikawa, Kojiro
AU  - Ichikawa K
FAU - Ohdo, Shigehiro
AU  - Ohdo S
FAU - Higuchi, Shun
AU  - Higuchi S
FAU - Yoshinari, Mototaka
AU  - Yoshinari M
FAU - Iida, Mitsuo
AU  - Iida M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Lysophosphatidylcholines)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitric Oxide Donors)
RN  - 0 (Nitro Compounds)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 0 (oxidized low density lipoprotein)
RN  - 14863-27-5 (We 201)
RN  - 5655-17-4 (stearoyl alpha-lysolecithin)
RN  - 9007-49-2 (DNA)
RN  - 92454-60-9 (FK 409)
RN  - EC 3.1.1.32 (Phospholipases A)
RN  - EC 3.1.1.4 (Phospholipases A2)
SB  - IM
MH  - Arteriosclerosis/blood/*etiology
MH  - Chemokine CCL2/genetics
MH  - DNA/metabolism
MH  - Diabetes Mellitus, Type 2/*blood
MH  - Endothelium, Vascular/metabolism
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Lipoproteins, LDL/*blood/chemistry/pharmacology
MH  - Lysophosphatidylcholines/*analysis/blood
MH  - NF-kappa B/metabolism
MH  - Nitric Oxide Donors/*pharmacology
MH  - Nitro Compounds/pharmacology
MH  - Phospholipases A/*metabolism
MH  - Phospholipases A2
MH  - RNA, Messenger/analysis
MH  - Thiobarbituric Acid Reactive Substances/analysis
MH  - Umbilical Veins
EDAT- 2003/03/21 04:00
MHDA- 2003/04/26 05:00
CRDT- 2003/03/21 04:00
PHST- 2003/03/21 04:00 [pubmed]
PHST- 2003/04/26 05:00 [medline]
PHST- 2003/03/21 04:00 [entrez]
AID - S0026049502052654 [pii]
AID - 10.1053/meta.2003.50049 [doi]
PST - ppublish
SO  - Metabolism. 2003 Mar;52(3):308-14. doi: 10.1053/meta.2003.50049.