© 1998 American Heart Association, Inc.
Original Contributions |
Modulation of Arachidonic Acid Release and Membrane Fluidity by Albumin in Vascular Smooth Muscle and Endothelial Cells
From the Department of Pharmacology, UMDS of Guy's and St Thomas's Hospitals, St Thomas's Campus, London, UK.
Correspondence to Dr S.V. Smirnov, Department of Pharmacology, UMDS of Guy's and St Thomas's Hospitals, St Thomas' Campus, Lambeth Palace Road, London SE1 7EH, United Kingdom. E-mail s.smirnov{at}umds.ac.uk
Abstract—Albumin is the
major plasma protein circulating in blood. Albumin potently
decreases capillary permeability, although the mechanisms are not
understood completely. Albumin also effectively binds
arachidonic acid (AA), which increases capillary
permeability. To investigate the interactions of BSA and AA with the
cell membrane, the effect of these substances on [3H]AA
release and membrane fluidity was studied in vascular myocytes and
endothelial cells. BSA (0.2 and 1 mg ·
mL-1) stimulated a significant release of
[3H]AA from both intact rat aorta and cultured smooth
muscle cells. This effect was not mimicked by 
-globulin or myoglobin
(both 1 mg · mL-1) in intact tissue. BSA, but not
-globulin and myoglobin, decreased the membrane fluidity (assessed
as changes in the steady-state fluorescence anisotropy of
1,6-diphenyl-1,3,5-hexatriene) in a concentration-dependent manner with
a half-maximum concentration between 0.007 and 0.4 mg ·
mL-1 in both freshly isolated and cultured rat aortic
myocytes and human umbilical vein endothelial cells. AA
(1 to 200 µmol/L) caused the opposite effect, increasing
membrane fluidity and antagonizing the effect of BSA. BSA modified at
its arginine residues, which are thought to be important in AA binding,
did not stimulate [3H]AA release and was significantly
less potent than native BSA in altering the membrane fluidity. The
effect of BSA can be explained by a high-affinity binding of AA to the
protein and extraction of AA from the cell membrane. The interaction
between BSA and AA could play a role in the regulation of vascular
permeability.
Key Words: vascular smooth muscle • endothelial cell • membrane fluidity • BSA • arachidonic acid
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