%0 Journal Article
%T Involvement of CD11b integrin in the alteration of metabolic factors after phorbol ester stimulation of human myeloid leukemia cells
%A Katharina Mandel
%A Anna Otte
%A Ralf Hass
%J Cell Communication and Signaling
%D 2012
%I BioMed Central
%R 10.1186/1478-811x-10-13
%X The human U937 myeloid leukemia cell line represents an in vitro model for monocyte/macrophage-like differentiation and retrodifferentiation [1-5]. A variety of molecular effects by differentiation-inducing agents such as the phorbol ester derivate 12-O-tetradecanoyl-phorbol-13-acetate (TPA) on cell adherence and filament expression in U937 cells have been extensively characterized [6,7]. Thus, the non-adherent growing and like tumor cells autonomously proliferating U937 wild-type population can be stimulated by TPA to differentiate along the monocyte/macrophage pathway which is associated with induced adherence and cessation of cell growth. The TPA-mediated attachment of differentiating U937 cells is accompanied by an enhanced expression of the ¦Â2-integrins CD11a, CD11c, CD18, and particularly CD11b [6]. These integrin compounds are cell membrane-associated glycoproteins whereby CD11a, CD11b and CD11c represent separate ¦Á-subunits to associate with the common ¦Â-subunit CD18, respectively. The appropriate heterodimeric protein complex forms a functional ¦Â2-integrin which is involved in the formation of cell-to-cell contacts and intercellular communication processes [8]. Moreover, junctional adhesion molecules including ICAMs can associate through their extracellular domains with functional ¦Â2-integrins on adjacent cells, contributing for example to the regulation of leukocyte-endothelial cell interactions [9].Previous work has demonstrated that a differentiation-defective subclone of the U937 cell line, termed TUR (TPA-U937-resistant), fails to express significant levels of CD11b after TPA treatment [10]. Concomitantly, these human TUR leukemia cells are unable to attach and continue to proliferate in response to a phorbol ester stimulation [11] indicating that CD11b displays a differentiation-associated function beyond an involvement in the regulation of cell attachment. Indeed, previous work has demonstrated that a down-modulation of the CD11b integrin fails to de
%K U937 leukemia cells
%K Differentiation
%K Adherence
%K Telomerase
%K Proteases
%K Signalling
%U http://www.biosignaling.com/content/10/1/13