Opposite effects of thrombospondin-1 via CD36 and CD47 on homotypic aggregation of monocytic cells

Procoagulant Platelets Form an α-Granule Protein-covered “Cap” on Their Surface That Promotes Their Attachment to Aggregates

“…In contrast, GPIb was more significantly concentrated in the cap, perhaps because of its known ability to bind to fibrin (30) or of the presence of VWF. Thrombospondin has been shown to bind to CD36 and to CD47 (31) and is known to form clusters on normal and Glanzmann thrombasthenia platelets, although these are smaller in the absence of fibrinogen (32). Thrombospondin incorporation is also known to improve fibrin clot formation (33).…”

Platelet-Derived Thrombospondin-1 Is Necessary for the Vitamin D-Binding Protein (Gc-Globulin) to Function as a Chemotactic Cofactor for C5a

“…U937 cells and neutrophils are capable of responding to TSP-1, because both cell types express CD36, CD47 and certain ␤ 1 integrins (35)(36)(37). Neutrophils also have been shown to express a significantly increased number of TSP-1 receptors after up-regulation from intracellular (specific) granules (30,38).…”

Induction of homotypic aggregation in the rainbow trout macrophage-like cell line, RTS11

“…The most studied inducers of HA in human myeloid cell lines have been PMA [7,8,10] and the ligation of specific clusters of differentiation (CD) [4,9]. There are fewer incidents of LPS and specific bacteria being shown to induce HA in U937 [5,6] but HA in response to synthetic RNA and zymosan appears to be a novel finding. As HA often accompanies the activation of immune cells [2], RTS11 might be a useful tool to screen for immunological stimuli in fish.…”

“…Cellular adhesion can be most conveniently studied in vitro, and human myeloid cell lines, such as U937, have been especially useful for studying HA [1,4e9]. Several treatments have been found to induce the HA of U937, but perhaps the most studied inducer has been phorbol 12-myristate 13-acetate (PMA) [6,8,10]. Some forms of protein kinase C and possibly protein tyrosine kinases also mediate HA of U937 [1].…”

“…Some forms of protein kinase C and possibly protein tyrosine kinases also mediate HA of U937 [1]. The surface molecules mainly responsible for HA appear to be the integrin leucocyte function-associated antigen-1 (LFA-1) interacting with its counter-receptor, the Ig superfamily member intercellular adhesion molecule-1 (ICAM-1) [5,6,11].…”