2024-03-29T04:37:59Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1524762021-07-20T11:30:10Zcom_10261_22com_10261_1col_10261_275
00925njm 22002777a 4500
dc
Molero, Cristina
author
Valverde, Ángela M.
author
Teruel, Teresa
author
Benito, Manuel
author
Lorenzo, Margarita
author
1996
[Background/Aims]: Hepatic phosphoenolpyruvate carboxykinase (PEPCK; EC 4.1.1.32) gene is absent in fetal liver. However, this gene can be initially expressed in 20-day-old fetal hepatocyte primary cultures under specific hormonal stimulation. The role of transcriptional factors involved is also studied. [Methods]: Primary 20-day-old fetal hepatocytes have been cultured and Northern-blot and nuclear run-on transcription assays have been performed. [Results]: Fetal hepatocytes in culture initially expressed PEPCK gene by dibutyryl cAMP, in the presence of dexamethasone. Dibutyryl cAMP increased by 8-fold the rate of transcription of PEPCK gene at 30 min, and produced a 50-fold increase in its mRNA content at 3 h. This induction of PEPCK expression by cAMP occurred in the presence of sustained levels of CCAAT/enhancer binding protein (C/EBP)α-δ mRNAs, and was accompanied by an increase in the rate of transcription and mRNA content of C/EBPβ gene, and a decrease in the expression of c-myc, in the absence of c-fos expression. In addition, insulin or phorbol esters decreased by 50% the PEPCK rate of transcription and its mRNA accumulation induced by dibutyryl cAMP This inhibitory effect of insulin or phorbol esters on PEPCK gene expression was accompanied by an increase in the rate of transcription and mRNA content of nuclear factors such as c-fos and c-myc, the expression of C/EBPs remaining essentially unmodified.
Journal of Hepatology 25(4): 510-517 (1996)
http://hdl.handle.net/10261/152476
10.1016/S0168-8278(96)80211-X
http://dx.doi.org/10.13039/501100004587
mRNA level
Phorbol esters
Transcription rate
PEPCK
Insulin
C/EBPs
C-Fos
c-myc
Dibutyryl cAMP
Fetal hepatocytes
Initial expression of phosphoenolpyruvate carboxykinase gene in fetal hepatocytes: Role of transcription factors