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Am J Physiol Cell Physiol (December 27, 2006). doi:10.1152/ajpcell.00401.2006
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Submitted on July 24, 2006
Accepted on December 22, 2006

CLASS A SCAVENGER RECEPTOR-MEDIATED CELL ADHESION REQUIRES THE SEQUENTIAL ACTIVATION OF LYN AND PI3-KINASE

Dejan Nikolic1, Jill M. Cholewa2, Cecelia Gass1, Ming Cui Gong3, and Steven R Post1*

1 Molecular and Biomedical Pharmacology, University of Kentucky, Lexington, Kentucky, United States
2 Nutritional Sciences, University of Kentucky, Lexington, Kentucky, United States
3 Physiology, University of Kentucky, Lexington, Kentucky, United States

* To whom correspondence should be addressed. E-mail: spost{at}uky.edu.

Class A scavenger receptors (SR-A) participate in multiple macrophage functions including macrophage adhesion to modified proteins. SR-A-mediated adhesion may therefore contribute to chronic inflammation by promoting macrophage accumulation at sites of protein modification. The mechanisms that couple SR-A binding to modified proteins with increased cell adhesion have not been defined. In this study, SR-A expressing HEK cells and SR-A+/+ or SR-A-/- macrophages were used to delineate the signaling pathways required for SR-A-mediated adhesion to modified protein. Inhibiting Gi/o activation, which decreases initial SR-A-mediated cell attachment, did not prevent the subsequent spreading of attached cells. In contrast, inhibition of Src kinases or PI3-kinase abolished SR-A-dependent cell spreading without affecting SR-A-mediated cell attachment. Consistent with these results, the Src kinase Lyn and PI3-kinase were sequentially activated during SR-A-mediated cell spreading. Furthermore, activation of both Lyn and PI3-kinase were required for enhancing paxillin phosphorylation. Activation of a Src kinase-PI3-kinase-Akt pathway was also observed in cells expressing a truncated SR-A protein that does not internalize indicating that SR-A-mediated activation of intracellular signaling cascades following adhesion to MDA-BSA is independent of receptor internalization. Thus, SR-A binding to modified protein activates signaling cascades that have distinct roles in regulating initial cell attachment and subsequent cell spreading.




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