PMID- 12535738
OWN - NLM
STAT- MEDLINE
DCOM- 20030604
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 166
IP  - 2
DP  - 2003 Feb
TI  - Electronegative LDL of FH subjects: chemical characterization and induction of 
      chemokine release from human endothelial cells.
PG  - 261-70
AB  - Electronegative LDL (LDL(-)) constitutes a plasma subfraction of LDL with 
      proinflammatory properties. Its proportion is increased in familial 
      hypercholesterolemia (FH); however, the characteristics of LDL(-) isolated from 
      FH subjects have not been previously studied. In this work, the composition, 
      oxidative status, and inflammatory capacity on endothelial cells of LDL(-) from 
      FH and normolipemic (NL) subjects were evaluated. LDL(-) from FH was relatively 
      enriched in esterified and free cholesterol and triglyceride, and had lower apoB 
      and phospholipid content compared with the non-electronegative fraction (LDL(+)). 
      LDL(-) also contained increased amounts of apoE, apoC-III, sialic acid, and 
      non-esterified fatty acids (NEFAs). The same was observed in NL subjects, except 
      that esterified cholesterol and phospholipid were similar in LDL(-) and LDL(+). 
      No difference was observed between the two fractions concerning malondialdehyde, 
      fatty acid hydroxides, and antioxidants, thereby indicating the absence of 
      increased oxidation of LDL(-) compared with LDL(+). When LDL(-) (100 mg/l) from 
      NL and FH subjects was incubated for 24 h with human umbilical vein endothelial 
      cells (HUVECs), interleukin 8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) 
      increased twofold in the culture medium compared with LDL(+). Vascular cell 
      adhesion molecule 1 (VCAM-1) expression was not increased by LDL(-). Our data 
      indicate that LDL(-) from FH or NL subjects shows no evidence of increased 
      oxidative modification compared to LDL(+); however, LDL(-) induces twofold the 
      release of chemokines by endothelial cells. This effect, which may contribute to 
      leukocyte recruitment and promote atherogenesis, may be greater in FH subjects in 
      which LDL(-) can be up to eightfold higher than in NL subjects.
FAU - Sanchez-Quesada, Jose Luis
AU  - Sanchez-Quesada JL
AD  - Servei de Bioquimica del Hospital de la Santa Creu i Sant Pau (HSCSP), C/Antoni 
      Maria Claret 167, 08025 Barcelona, Spain.
FAU - Camacho, Mercedes
AU  - Camacho M
FAU - Anton, Rosa
AU  - Anton R
FAU - Benitez, Sonia
AU  - Benitez S
FAU - Vila, Lluis
AU  - Vila L
FAU - Ordonez-Llanos, Jordi
AU  - Ordonez-Llanos J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
SB  - IM
MH  - Blotting, Western
MH  - Cells, Cultured
MH  - Chemokine CCL2/analysis
MH  - Endothelium, Vascular/*cytology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Hyperlipoproteinemia Type II/*blood/*physiopathology
MH  - Interleukin-8/analysis
MH  - Lipoproteins, LDL/*analysis/*chemistry
MH  - Probability
MH  - Reference Values
MH  - Statistics, Nonparametric
MH  - Vascular Cell Adhesion Molecule-1/*analysis
EDAT- 2003/01/22 04:00
MHDA- 2003/06/05 05:00
CRDT- 2003/01/22 04:00
PHST- 2003/01/22 04:00 [pubmed]
PHST- 2003/06/05 05:00 [medline]
PHST- 2003/01/22 04:00 [entrez]
AID - S0021-9150(02)00374-X [pii]
AID - 10.1016/s0021-9150(02)00374-x [doi]
PST - ppublish
SO  - Atherosclerosis. 2003 Feb;166(2):261-70. doi: 10.1016/s0021-9150(02)00374-x.