| Literature DB >> 10388540 |
A G van Velzen1, H Suzuki, T Kodama, T J van Berkel.
Abstract
Scavenger receptor class A (SR-A) facilitates the development of atherosclerosis, 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 cells). In resident PM no effect of the absence or presence of SR-A on cell adhesion was observed, either in the presence or in the absence of serum. However, 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 influenced 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 appears that under these conditions SR-A does contribute to adhesion, since both 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 divalent-cation-independent adhesion of activated PM and Kupffer cells, suggesting that SR-A may influence the residence time of cells at sites of cellular activation, e.g., in atherosclerotic plaques and during liver infection. Copyright 1999 Academic Press.Entities:
Mesh:
Substances:
Year: 1999 PMID: 10388540 DOI: 10.1006/excr.1999.4530
Source DB: PubMed Journal: Exp Cell Res ISSN: 0014-4827 Impact factor: 3.905