Human calpactin II (lipocortin I) messenger ribonucleic acid is not induced by glucocorticoids.

Abstract

Studies were carried out to examine the effect of glucocorticoids on human calpactin II (lipocortin I) mRNA expression. A cRNA probe for human calpactin II (hCPII) was used in a solution hybridization assay to study the effect of dexamethasone on hCPII mRNA levels in human skin fibroblasts, peripheral lymphocytes, pulmonary alveolar macrophages, and HeLa S3 cells. As a positive control, human metallothionein II (hMTII) mRNA levels were measured since hMTII is known to be regulated by glucocorticoids and heavy metals, both of which induce transcriptional activity of the gene. Dexamethasone treatment of these human cell types caused a dose-dependent increase in hMTII mRNA levels, whereas no effect on hCPII mRNA levels was observed. These findings were confirmed in time course studies, where 10(-6) M dexamethasone treatment caused a maximal 2- to 5-fold increase in hMTII mRNA levels after 6-8 h of treatment but no increase in hCPII mRNA levels was observed at any time point up to 24 h. A human glucocorticoid sensitive lymphoid cell line, CEM C7, and a glucocorticoid resistant mutant, ICR-27, isolated from CEM C7, were included in order to confirm the requirement of a functional glucocorticoid receptor (GR) in the induction of glucocorticoid-regulated genes. Dexamethasone (10(-6) M) induced hMTII but not hCPII mRNA in CEM C7 cells, whereas neither hMTII nor hCPII mRNA was induced in ICR-27 cells. In conclusion, our data suggest that glucocorticoids do not induce calpactin II (lipocortin I) mRNA in the human cell types studied.