PMID- 16753331
OWN - NLM
STAT- MEDLINE
DCOM- 20061208
LR  - 20181201
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1761
IP  - 9
DP  - 2006 Sep
TI  - Wide proinflammatory effect of electronegative low-density lipoprotein on human 
      endothelial cells assayed by a protein array.
PG  - 1014-21
AB  - Electronegative low-density lipoprotein (LDL(-)) is a modified subfraction of LDL 
      present in plasma able to induce the release of interleukin 8 (IL-8) and monocyte 
      chemotactic protein 1 (MCP-1) by human umbilical vein endothelial cells (HUVEC). 
      To ascertain whether further inflammation mediator release could be induced by 
      LDL(-), a protein array system was used to measure 42 cytokines and related 
      compounds. Native LDL and LDL(-) isolated from normolipemic subjects were 
      incubated for 24 h with HUVEC and culture supernatants were used to measure 
      inflammation mediator release. The protein array revealed that IL-6, 
      granulocyte/monocyte colony-stimulating factor (GM-CSF) and growth-related 
      oncogene (GRO) release were increased by cultured HUVEC in response to LDL(-). 
      LDL(-) enhanced production of IL-6 (4-fold vs. LDL(+)), GM-CSF (4-fold), GRObeta 
      (2-fold) and GROgamma (7-fold) was confirmed by ELISA. Time-course experiments 
      revealed that IL-6 was released earlier than the other inflammation mediators, 
      suggesting a first-wave cytokine action. However, the addition of IL-6 alone did 
      not stimulate the production of IL-8, MCP-1 or GM-CSF. Moreover, IL-8, MCP-1 or 
      GM-CSF alone did not promote the release of the other inflammatory molecules. 
      Modification of LDL(+) by phospholipase A(2)-mediated lipolysis or by loading 
      with non-esterified fatty acids (NEFA) reproduced the action of LDL(-), thereby 
      suggesting the involvement of NEFA and/or lysophosphatidylcholine in the release 
      of these molecules. Our results indicate that LDL(-) promotes a proinflammatory 
      phenotype in endothelial cells through the production of cytokines, chemokines 
      and growth factors.
FAU - Benitez, Sonia
AU  - Benitez S
AD  - Department of Biochemistry and Institut de Recerca, Hospital de la Santa Creu i 
      Sant Pau, C/Antoni Maria Claret 167, 08025 Barcelona, Spain.
FAU - Camacho, Mercedes
AU  - Camacho M
FAU - Bancells, Cristina
AU  - Bancells C
FAU - Vila, Luis
AU  - Vila L
FAU - Sanchez-Quesada, Jose Luis
AU  - Sanchez-Quesada JL
FAU - Ordonez-Llanos, Jordi
AU  - Ordonez-Llanos J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060401
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cytokines)
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipoproteins, LDL)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - EC 3.1.1.32 (Phospholipases A)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokines, CXC/metabolism
MH  - Cytokines/*metabolism
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Fatty Acids, Nonesterified/*pharmacology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
MH  - Humans
MH  - Inflammation/metabolism
MH  - Interleukin-6/metabolism
MH  - Lipoproteins, LDL/pharmacology/*physiology
MH  - Phospholipases A/metabolism
MH  - Protein Array Analysis
MH  - Umbilical Veins/cytology
EDAT- 2006/06/07 09:00
MHDA- 2006/12/12 09:00
CRDT- 2006/06/07 09:00
PHST- 2005/09/20 00:00 [received]
PHST- 2006/03/17 00:00 [revised]
PHST- 2006/03/27 00:00 [accepted]
PHST- 2006/06/07 09:00 [pubmed]
PHST- 2006/12/12 09:00 [medline]
PHST- 2006/06/07 09:00 [entrez]
AID - S1388-1981(06)00098-9 [pii]
AID - 10.1016/j.bbalip.2006.03.020 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2006 Sep;1761(9):1014-21. doi: 
      10.1016/j.bbalip.2006.03.020. Epub 2006 Apr 1.