Albumin and Antioxidants Inhibit Serum-deprivation-induced Cell Adhesion in Hematopoietic Cells

Abstract

− Previously, we identified albumin as an inhibitory factor in serum for cell adhesion of T cells such as human Jurkat T and primary cultured human T cells. In the present study, we found that other hematopoietic cell lines including U-937 human monocytes, THP-1 human monocytes, K-562 promyelocytic leukemia cells, and HL-60 human leukemia cells, also adhere to tissue culture flasks when serum is withdrawn, and albumin exerts an inhibitory effect on cell adhesion by those cells, implying that this inhibition is a common phenomenon in hematopoietic cells. Furthermore, we found that cell adhesion is inhibited by antioxidants such as (-)-epigallocatechin-3-gallate (EGCG), morin, and a-tocopherol. Our results suggest that albumin may inhibit basal cell adhesion of hematopoietic cells and that the oxidative balance in the plasma may be important for cell adhesion of hematopoietic cells in vivo.

Cell-permeable ceramides act as novel regulators of U937 cell–cell adhesion mediated by CD29, CD98, and CD147

“…Cell adhesion events are required for cell localization, effector recognition, and activation phenomena, as demonstrated between T cells and antigen-presenting cells, cytotoxic T cells and their targets, and lymphocytes and endothelium (Kim 2008;Kinashi and Katagiri 2004); b1-integrins (CD29) are key adhesion molecules in modulating various cell-cell and cell-matrix adhesions, and over-activation of these molecules (Tsurudome and Ito 2000;Han et al 2008) and subsequent up-regulation of cell adhesion are known to play a critical role in the onset of various diseases, such as cancers, and inflammatory and autoimmune diseases (Gascoigne et al 2003;Haylock and Nilsson 2006). This notion led us to the hypothesis that the blockade of CD29 activation could therefore be a therapeutic target for the suppression of relevant diseases (Salmaso et al 2002).…”