Glucocorticoid induction of CRE-binding protein isoform mRNAs in rat C6 glioma cells

Jungmann, Richard A.; Wang, Xuesong; Milkowski, Deborah M.; Short, Marc L.

doi:10.1093/nar/20.4.825

Cited by 19 publications

(8 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, direct interactions between the cAMP-dependent pathway and steroid receptor activation may be operative in modulating gene expression. In addition, the synthesis of the cAMP-responsive element binding protein that mediates the cAMP-induced changes in gene transcription is markedly increased by dexamethasone ( 18). Our data, however, do not distinguish between these possibilities leaving presently unanswered the question of whether the dexamethasone-cAMP combination affects insulin gene transcription through a transcriptional, a posttranscriptional, or both mechanisms.…”

Section: Methodscontrasting

confidence: 63%

“…However, it is unlikely that such a lack ofinhibitory effect alone could account for the 40% increase in the steady state levels of insulin mRNA we oW served. Rather, it is most likely that this net increase reflects also the involvement of other positive factors, such as the increased synthesis of the cAMP-responsive element binding protein ( 18). Because the regulation of the insulin gene is defective in dispersed islet cells, these factors should be somehow dependent on the maintenance ofthe contacts : cells normally establish within the islets ofLangerhans.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Cyclic adenosine monophosphate prevents the glucocorticoid-mediated inhibition of insulin gene expression in rodent islet cells.

Philippe¹,

Giordano²,

Gjinovci³

et al. 1992

J. Clin. Invest.

View full text Add to dashboard Cite

Dexamethasone negatively regulates insulin gene expression in HIT-15 cells. In vivo, however, an excess of glucocorticoids results in an increase in insulin biosynthesis and peripheral hyperinsulinemia. To resolve this contradiction, we have studied the effects of dexamethasone in primary rat islet cells. We show here that dexamethasone decreases insulin mRNA levels in single islet cells, as in HIT-15 cells, but does not affect these levels in reaggregated islet cells and increases them in intact islets of Langerhans. Because cAMP is an important regulator of insulin gene expression and intracellular cAMP content may be decreased in single (3 cells, we investigated whether cAMP could prevent the inhibitory effect of dexamethasone on insulin mRNA levels. In the presence of cAMP analogues, the inhibitory action of dexamethasone was not only prevented, but insulin mRNA increased to levels comparable to those observed when cAMP analogues were used alone. We conclude that the insulin gene is negatively regulated by dexamethasone in single islet cells, but that other factors such as cAMP prevent this effect when the native environment of islet cells is preserved. Our results indicate that insulin gene regulation is influenced by cell to cell contacts within the islet, and that intracellular cAMP levels might be influential in this regulation. (J. Clin. Invest. 1992. 90:2228-2233

show abstract

Section: Methodscontrasting

confidence: 63%

Section: Methodsmentioning

confidence: 99%

Cyclic adenosine monophosphate prevents the glucocorticoid-mediated inhibition of insulin gene expression in rodent islet cells.

Philippe¹,

Giordano²,

Gjinovci³

et al. 1992

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Jungmann et al . [38] showed that glucocorticoids induce the CREB isoform mRNA in rat C6 glioma cells, but counteract the induction of lactate dehydrogenase by cAMP. Many different transcription factors can also bind to CRE.…”

Section: Discussionmentioning

confidence: 99%

CREB is involved in mouse annexin A1 regulation by cAMP and glucocorticoids

Antonicelli

Coupade

Russo‐Marie

et al. 2001

European Journal of Biochemistry

View full text Add to dashboard Cite

A cAMP and some glucocorticoid response elements have been underlined in the promoter of mouse annexin A1. To analyse the function of these DNA sequences, the role of cAMP and glucocorticoids, as well as the transcription factors involved in their activation, were investigated. A construct containing 1381 bp of the DNA 5 H -flanking annexin A1 gene fused to LacZ was used. The level of activation of the reporter gene was analysed by transient transfection of the JEG3 cell line. Activation of b-galactosidase expression was observed with both dibutyryl cAMP and dexamethasone when compared with cells treated with serum only. Simultaneous addition of dexamethasone and dibutyryl cAMP did not result in a synergistic effect but rather in a competitive one. Gel-shift assays with a probe including the cAMP response element-like element of the annexin A1 promoter revealed a main specific DNA±protein complex when cells were stimulated with dibutyryl cAMP and/or dexamethasone. In all cases CREB protein was identified by supershift analysis. We therefore conclude that this cAMP response element sequence plays a prominent role in the transactivation of the annexin A1 promoter by dibutyryl cAMP and that it is involved in the response to glucocorticoids.

show abstract

“…The cytosolic and particulate fractions were also assayed for the presence of CRE-binding proteins. CREB is constitutively expressed in C6 (Jungmann et al, 1992), and its level rapidly decreased in both fractions on stimulation with dbcAMP ( Fig. 6B).…”

Section: Cellular Distribution and Activity Of Pkamentioning

confidence: 94%

Cyclic AMP-mediated induction of the glial fibrillary acidic protein is independent of protein kinase A activation in rat C6 glioma

et al. 1997

View full text Add to dashboard Cite

N6-O'2-dibutyryl cAMP (dbcAMP), N6-monobutyryl cAMP (N6-mbcAMP), 8-Chloro cAMP (ClcAMP), and O'2-monobutyryl cAMP (O'2-mbcAMP) were used to study glial fibrillary acidic protein (GFAP) induction in rat C6 glioma. With the exception of O'2-mbcAMP, these cAMP analogs induced GFAP after stimulation of cells with a concentration of 0.5-1 mM. Only dbcAMP and N6-mbcAMP increased the intracellular concentration of cAMP. Protein kinase A (PKA) activation is often proposed to be involved in GFAP expression in astrocytes. Ion-exchange chromatography indicated that protein kinase activity is associated with PKA type II in C6. dbcAMP, N6-mbcAMP, and ClcAMP upregulated the amount of cAMP-binding proteins approximately twofold. RI was upregulated in the cytosol and particulate fraction, whereas RII was not affected after stimulation with dbcAMP. Concomitant, the PKA activity decreased approximately 60% and 40% in the cytosol and particulate fraction, respectively. CREB is constitutively expressed in C6 and is downregulated after stimulation with dbcAMP. The membrane-permeable PKA inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89) did not suppress the induction of GFAP-mRNA and its translation into GFAP. On the contrary, depending on the time difference between H89 and dbcAMP addition to C6, GFAP synthesis could even be potentiated more than twofold. Experiments in the presence of cycloheximide showed that protein synthesis is necessary for GFAP transcription. Although all components of the PKA signal transduction pathway are present in C6, GFAP synthesis is not dependent on PKA activation but required the synthesis of an unidentified factor.

show abstract

Glucocorticoid induction of CRE-binding protein isoform mRNAs in rat C6 glioma cells

Cited by 19 publications

References 30 publications

Cyclic adenosine monophosphate prevents the glucocorticoid-mediated inhibition of insulin gene expression in rodent islet cells.

Cyclic adenosine monophosphate prevents the glucocorticoid-mediated inhibition of insulin gene expression in rodent islet cells.

CREB is involved in mouse annexin A1 regulation by cAMP and glucocorticoids

Cyclic AMP-mediated induction of the glial fibrillary acidic protein is independent of protein kinase A activation in rat C6 glioma

Contact Info

Product

Resources

About