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* William Harvey Research Institute,
Rheumatology Unit, Guy’s, St. Thomas, and King’s College School of Medicine, and
Department of Neuroendocrinology, Imperial College School of Medicine, London, United Kingdom
The effect of the glucocorticoid inducible protein annexin 1
(ANXA1) on the process of monocytic cell migration was studied using
transfected U937 cells expressing variable protein levels. An antisense
(AS) (36.4AS; 
50% less ANXA1) and a sense (S) clone (15S;
overexpressing the bioactive 24-kDa fragment) together with the empty
plasmid CMV clone were obtained and compared with wild-type U937 cells
in various models of cell migration in vitro and in vivo.
15S-transfected U937 cells displayed a reduced (50%) degree of
trans-endothelial migration in response to stromal
cell-derived factor-1
(CXC chemokine ligand 12 (CXCL12)). In
addition, the inhibitory role of endogenous ANXA1 on U937 cell
migration in vitro was confirmed by the potentiating effect of a
neutralizing anti-ANXA1 serum. Importantly, overexpression of ANXA1
in clone 15S inhibited the extent of cell migration into rheumatoid
synovial grafts transplanted into SCID mice. ANXA1 inhibitory effects
were not due to modifications in adhesion molecule or CXCL12 receptor
(CXCR4) expression as shown by the similar amounts of surface molecules
found in transfected and wild-type U937 cells. Likewise, an equal
chemotactic response to CXCL12 in vitro excluded an intrinsic defect in
cell motility in clones 15S and 36.4AS. These data strongly support the
notion that ANXA1 critically interferes with a leukocyte endothelial
step essential for U937 cell, and possibly monocyte, transmigration
both in vitro and in vivo.
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