Increase in epidermal growth factor receptor and its mRNA levels by parathyroid hormone (1-34) and parathyroid hormone-related protein (1-34) during differentiation of human trophoblast cells in culture

1993 ◽  
Vol 53 (1) ◽  
pp. 32-42 ◽  
Author(s):  
Eliane Alsat ◽  
Jocelyne Haziza ◽  
Marie-Louise Scippo ◽  
Francis Frankenne ◽  
Danièle Evain-Brion
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Mrna Levels ◽  
Related Protein ◽  
Human Trophoblast ◽  
Parathyroid Hormone Related Protein ◽  
Epidermal Growth ◽  
Human Trophoblast Cells

Normal epidermal growth factor receptor signaling is dispensable for bone anabolic effects of parathyroid hormone

Bone ◽  
2012 ◽  
Vol 50 (1) ◽  
pp. 237-244 ◽  
Author(s):  
Marlon R. Schneider ◽  
Maik Dahlhoff ◽  
Olena Andrukhova ◽  
Jessica Grill ◽  
Martin Glösmann ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Signaling ◽  
Epidermal Growth ◽  
Growth Factor Receptor Signaling

scholarly journals Epidermal growth factor-stimulated parathyroid hormone-related protein expression involves increased gene transcription and mRNA stability

1995 ◽  
Vol 307 (1) ◽  
pp. 159-167 ◽  
Author(s):  
J K Heath ◽  
J Southby ◽  
S Fukumoto ◽  
L M O'Keeffe ◽  
T J Martin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Gene Transcription ◽  
Mrna Stability ◽  
Specific Effect ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Epidermal Growth

Epidermal growth factor (EGF) produced rapid and striking effects on parathyroid hormone-related protein (PTHrP) gene expression in the immortalized human keratinocyte cell line, HaCaT. Steady-state levels of PTHrP mRNA and secreted PTHrP were increased 10-fold by maximally effective concentrations of EGF. EGF increased both PTHrP gene transcription and PTHrP mRNA stability. Nuclear run-on assays demonstrated a 4-fold increase in transcriptional rate in EGF-stimulated cells while transient transfection analysis indicated that the action of EGF on transcription involved both the GC-rich promoter, P2, and the downstream TATA promoter, P3, but apparently not the upstream TATA promoter, P1. In experiments where EGF treatment produced more stable PTHrP transcripts, the half-life of c-fos mRNA was unaltered, suggesting a relatively specific effect of EGF. Moreover, only those species of PTHrP mRNA containing two of the alternative 3′ exons (exons VII and VIII) were stable, those containing exon IX were not. Reverse-transcription PCR demonstrated that EGF produced differential increases in the abundance of PTHrP mRNA species initiated by the three PTHrP promoters. The major effect was seen on the abundance of transcripts initiated by P1 and P2, with less marked regulation of P3-initiated transcripts. Thus EGF regulation of PTHrP gene expression in HaCaT cells is multifactorial and the combination of its actions at the 5′ and 3′ ends of the gene favours the accumulation of subpopulations of PTHrP mRNA containing exons I, VII and VIII.

scholarly journals Regulation of parathyroid hormone-related protein gene expression by epidermal growth factor-family ligands in primary human keratinocytes

2004 ◽  
Vol 181 (1) ◽  
pp. 179-190 ◽  
Author(s):  
YM Cho ◽  
DA Lewis ◽  
PF Koltz ◽  
V Richard ◽  
TA Gocken ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Reporter Gene ◽  
Human Keratinocytes ◽  
Mrna Levels ◽  
Related Protein ◽  
Primary Keratinocytes ◽  
Primary Human Keratinocytes ◽  
Parathyroid Hormone Related Protein ◽  
Epidermal Growth

Cultured primary human keratinocytes were the first non-cancer-derived cell type reported to produce the humoral hypercalcemia factor, parathyroid hormone-related protein (PTHrP). Emerging evidence suggests that only a subset of keratinocytes produce high levels of PTHrP in vivo. We found that the PTHrP mRNA content of intact human skin was minimal, whereas transcripts were easily detectable in primary keratinocytes derived from those skin samples. We hypothesized that conditions associated with growth in culture activated PTHrP gene expression in primary keratinocytes. In culture, keratinocytes produce a number of epidermal growth factor (EGF)-like ligands (transforming growth factor-alpha, heparin binding-EGF and amphiregulin) and their receptor, ErbB1. Treatment of keratinocytes with a specific erbB1 inhibitor (PD153035) reduced PTHrP mRNA levels by >80% in rapidly growing keratinocytes. Treatment of keratinocytes with reagents that neutralize amphiregulin reduced PTHrP mRNA levels by approximately 60%. Blockade of erbB1 signaling reduces transcription from the endogenous PTHrP P3-TATA promoter. The Ets transcription factor-binding site, 40 bases upstream of the P3 promoter, is required for baseline expression of PTHrP reporter gene constructs in keratinocytes; in addition, cotransfection of Ets-1 and Ets-2 expression vectors activate the reporter gene constructs. Finally, disruption of both ras and raf signaling reduce reporter gene expression by 80%, suggesting that ErbB1 signaling is mediated by the classic ras/MAP kinase pathway. These findings suggest that acquisition of EGF-like ligand expression has the potential to substantially activate PTHrP gene expression in the epidermis.

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