Published Online
on June 23, 2003

A more recent version of this article appeared on July 8, 2003

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Submitted on January 23, 2003
Revised on March 25, 2003
Accepted on March 26, 2003

Platelet-Activating Factor Acetylhydrolase Is Mainly Associated With Electronegative Low-Density Lipoprotein Subfraction

Sonia Benítez PhD, José Luis Sánchez-Quesada PhD, Vicent Ribas BSc, Oscar Jorba BSc, Francisco Blanco-Vaca MD, PhD, Francesc González-Sastre MD, PhD, and Jordi Ordóñez-Llanos MD, PhD^*

From the Servei de Bioquímica and Institut de Recerca (S.B., J.L.S.-Q., V.R., O.J., F.B.-V., F.G.-S., J.O.-L.), Hospital de la Santa Creu i Sant Pau, and Departament de Bioquímica i Biología Molecular (F.G.-S., J.O.-L.), Universitat Autònoma de Barcelona, Barcelona, Spain.

^* To whom correspondence should be addressed. E-mail: jordonez{at}hsp.santpau.es.

Background--Electronegative LDL [LDL(-)], a modified subfraction of LDL present in plasma, induces the release of interleukin-8 and monocyte chemotactic protein-1 from cultured endothelial cells.

Methods and Results--We demonstrate that platelet-activating factor acetylhydrolase (PAF-AH) is mainly associated with LDL(-). LDL(-) had 5-fold higher PAF-AH activity than the nonelectronegative LDL subfraction [LDL(+)] in both normolipemic and familial hypercholesterolemic subjects. Western blot analysis after SDS-PAGE confirmed these results, because a single band of 44 kDa corresponding to PAF-AH appeared in LDL(-) but not in LDL(+). Nondenaturing polyacrylamide gradient gel electrophoresis demonstrated that PAF-AH was bound to LDL(-) regardless of LDL size. In accordance with the above findings, nonesterified fatty acids, a cleavage product of PAF-AH, were increased in LDL(-) compared with LDL(+).

Conclusions--The high PAF-AH activity observed in LDL(-) could be related to the proinflammatory activity of these lipoproteins toward cultured endothelial cells.

Key words: lipoproteins • inflammation • fatty acids

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