Prednisolone induced surface alterations in HeLa cells

A comparison of the effects of prednisolone and methylprednisolone on human lymphoblastoid cells

“…It is generally accepted that glucocorticoid hormones exert their effects by binding to cytoplasmic receptor proteins, which mediate their translocation to the nucleus, where they alter gene activity (Jensen & De Sombre, 1973), but there is no evidence that this is the mechanism of action in the effects that we have observed. However, there is evidence that the cell surface may be one target for the direct action of steroids (Dell'Orco & Melnykovych, 1970;Fiskin & Melnykovych, 1971;Plagemann & Renner, 1972), and it has also been suggested that, in corticosteroid-sensitive rodent cells, the hormone causes an alteration in some undefined key membrane property (Stevens et al, 1974). It seems that in our system there is a direct interaction between the steroid and the cell surface to produce inhibition of uptake ofnucleosides 324 A. W. WADDELL AND A. R. CURRIE 1.0 1.5 2.0 0.5 1.0 1.5 2.0 0.5 1.0 1.5 2.0 [Steroid] (mM) Fig.…”

Cell Proliferation and DNA Dependent DNA Polymerase Estimation in Acute Lymphoblastic Leukaemia during Treatment with Prednisone and Vincristine

“…In 1 patient, a certain transformation to more 'mature lymphoid' cells from lymphoblasts was seen. It is known that prednisone can induce ultrastructural changes in normal lymphocytes as well as surface alterations in HeLa cells (Fiskin & Melnykovych 1971, Werthamer & Amaral 1975. The exact mechanism of this is far from understood.…”

Effect of methylprednisolone on the nucleoside metabolism of a human lymphoblastoid cell line

“…There is, however, evidence for the cell surface as a target for glucocorticoids (Dell'Orco and Melnykovych, 1970;Fiskin and Melnykovych, 1971;Plagemann and Renner, 1972). Since the effects we observe occur at MPS concentrations 10,000 x those which saturate cytoplasmic receptors (Bird et al, 1975) and these effects appear to be independent of receptor concentrations, we consider that the inhibition of nucleoside transport demonstrated here is not receptormediated.…”