Posttranscriptional mechanisms of glucocorticoid antiproliferative effects: glucocorticoids inhibit IL-6-induced proliferation of B9 hybridoma cells.

Abstract:

:Addition of rIL-6 to IL-6-dependent B9 cells starved for IL-6 for 16-20 h stimulated a vigorous proliferative response. Glucocorticoids (GCs), in a concentration-dependent manner, inhibited rIL-6-stimulated proliferation of B9 cells This inhibition was specific for the GCs, evident by the capacity of the GCs, dexamethasone, prednisolone, and hydrocortisone, but not non-GC steroids, to suppress rIL-6-dependent B9 cell proliferation. Furthermore, GC inhibition of IL-6-stimulated B9 cell proliferation was receptor mediated and was abrogated by the GC receptor antagonist, RU486. In addition to their reported effects on inhibition IL-6 expression, the results presented support the notion that GCs also acted distally by suppressing signal transduction through the IL-6 receptor.

journal_name

Cell Transplant

journal_title

Cell transplantation

authors

Almawi WY,Tamim H

subject

Has Abstract

pub_date

2001-03-01 00:00:00

pages

161-4

issue

2

eissn

0963-6897

issn

1555-3892

journal_volume

10

pub_type

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