The role of scavenger receptor class A in the adhesion of cells is dependent on cell type and cellular activation state

Citation
Ag. Van Velzen et al., The role of scavenger receptor class A in the adhesion of cells is dependent on cell type and cellular activation state, EXP CELL RE, 250(1), 1999, pp. 264-271
Citations number
32
Categorie Soggetti
Cell & Developmental Biology
Journal title
EXPERIMENTAL CELL RESEARCH
ISSN journal
00144827 → ACNP
Volume
250
Issue
1
Year of publication
1999
Pages
264 - 271
Database
ISI
SICI code
0014-4827(19990710)250:1<264:TROSRC>2.0.ZU;2-Z
Abstract
Scavenger receptor class A (SR-A) facilitates the development of atheroscle rosis, which might be due to its role in the uptake of modified low-density lipoproteins. However, the receptor is also suggested to be important for cell adhesion, thereby potentially influencing the residence time of cells in vivo. Using SR-A-deficient mice, we investigated the role of SR-A in the adhesion of peritoneal macrophages (PM) and tissue macrophages (Kupffer ce lls). In resident PM no effect of the absence or presence of SR-A on cell a dhesion was observed, either in the presence or in the absence of serum. Ho wever, in thioglycollate-induced PM, SR-A is important for adhesion both in the presence and in the absence of serum and more than 85% of the divalent -cation-independent adhesion in the presence of serum is mediated by SR-A. In unactivated Kupffer cells, like in resident PM, adhesion is not influenc ed by the absence or presence of SR-A. In vivo administration of phorbol 12 -myristate 13-acetate leads to the activation of Kupffer cells, and it appe ars that under these conditions SR-A does contribute to adhesion, since bot h in the absence and in the presence of serum SR-A is responsible for about 35% of cell adhesion. It is concluded that SR-A is important for the dival ent-cation-independent adhesion of activated PM and Kupffer cells, suggesti ng that SR-A may influence the residence time of cells at sites of cellular activation, e.g., in atherosclerotic plaques and during liver infection. ( C) 1999 Academic Press.