Dimethyl sulfoxide decreases specific EGF binding

Abstract

Dimethyl sulfoxide (DMSO) stimulates tyrosine phosphorylation of the hepatic EGF receptor in isolated membrane preparations. To determine whether DMSO affects EGF binding, primary cultures of rat hepatocytes were incubated with 1-10% DMSO for 30 min prior to the addition of 125I-EGF. DMSO (1-2%) reduced specific 125I-EGF binding; the effect was maximal (a 40-60% reduction) at 5-7.5% DMSO and was reversed by removing the DMSO. Scatchard analysis showed that the reduction in binding was due to a change in receptor affinity. The decrease in binding was not seen when other, slightly less polar, solvents (eg, acetone and ethanol) were tested. DMSO also reduced 125I-EGF binding to purified rat liver plasma membranes. This reduction was seen in the absence of added ATP and in membranes that had been pretreated with TLCK, a tyrosine kinase inhibitor. Thus, completion of the receptor autophosphorylation reaction was not necessary to effect the change. The data are consistent with a DMSO-induced alteration of receptor conformation that reversibly reduces receptor affinity.

Inhibition of distinct steps in the adipocyte differentiation pathway in 3T3 T mesenchymal stem cells by dimethyl sulphoxide (DMSO)

“…1990, Srinivas, Sironmani & Shanmugam 1991. In addition, DMSO-induced inhibition of DNA synthesis in primary hepatocyte cultures may involve an interference with the function of growth factor receptors or post-receptor signal transduction components (Earp, Lin & Blaisdell 1984, Kost & Michalopoulos 1991.…”

Effect of dimethyl sulfoxide on mouse embryo fibroblasts: inhibition of plasminogen activator inhibitor deposition and interference with early events of serum‐stimulated growth

“…The primary effect of DMSO on cultured cells appears to be on the cell membrane and such an effect was shown to interfere with the binding of EGF with its receptor [12]. Alteration of membrane conformation may change the transport properties of the membrane.…”

“…An increase in the phosphotidylinositol turnover, phosphorylation of proteins, autophosphorylation of growth factor receptors, increase in intracellular pH and Ca 2+, rearrangement of actin bundles, increase in nutrient transport and enhanced RNA synthesis are some of the consequences of serumstimulated growth [34,41]. DMSO has been reported to stimulate tyrosine residue phosphorylation of epidermal growth factor (EGF) receptor and subsequently shown to affect the binding of EGF to its receptor [12]. The DMSOmediated reduced binding of EGF to its receptor may result in the inhibition of DNA synthesis.…”

“…The polar solvent has been shown to increase the adhesiveness of low metastatic clones of 3LL carcinoma [6]. DMSO treatment enchanced albumin production in transformed hepatocytes [9], and decreased the binding of EGF to its receptor [12]. DMSO treatment enchanced albumin production in transformed hepatocytes [9], and decreased the binding of EGF to its receptor [12].…”

“…These effects were accompanied by reduced tumorigenecity and reversal of the malignant phenotype of cells to normal phenotype [7][8][9][10][11]. DMSO treatment enchanced albumin production in transformed hepatocytes [9], and decreased the binding of EGF to its receptor [12]. The production of plasminogen activator in human carcinoma was inhibited by DMSO [5].…”