Cellular localization of immunoreactive epidermal growth factor during Wolffian duct differentiation of the fetal mouse

1997 ◽  
Vol 25 (4) ◽  
pp. 277-281 ◽  
Author(s):  
C. Gupta
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cellular Localization ◽  
Wolffian Duct ◽  
Fetal Mouse ◽  
Epidermal Growth

scholarly journals The effect of epidermal growth factor (EGF) on the differentiation of the rough endoplasmic reticulum in fetal mouse small intestine in organ culture.

1981 ◽  
Vol 29 (6) ◽  
pp. 765-770 ◽  
Author(s):  
J F Beaulieu ◽  
R Calvert
Keyword(s):  
Endoplasmic Reticulum ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Organ Culture ◽  
Rough Endoplasmic Reticulum ◽  
Fetal Mouse ◽  
Absorptive Cells ◽  
Mouse Small Intestine ◽  
Epidermal Growth ◽  
Mouse Fetuses

The differentiation of the rough endoplasmic reticulum (RER) of mouse duodenal absorptive cells located at the tip of the villi at 17 days of gestation was compared to that of absorptive cells in duodenal explants of 15-day-old mouse fetuses cultured for 72 hr 1) with Trowell T8 medium (without insulin) alone or supplemented 2) with epidermal growth factor (EGF; 100 ng/ml) or 3) with 25% bovine amniotic fluid (BAF). Glucose-6-phosphatase activity (G6Pase) was localized cytochemically to ensure a better identification of the RER. The intersections of a double lattice falling over and outside the RER were counted and the percentage of intersections over the RER was estimated. With this method, the extent of the RER is not statistically different when the absorptive cells in utero are compared to those of explants cultured with EGF. However, the extent of the RER in the absorptive cells cultured with Trowell T8 medium alone or supplemented with BAF is 50% lower than in the former two groups. It is concluded that EGF promotes the maturation of duodenal absorptive cells in organ culture.

scholarly journals Detection of epidermal growth factor-urogastrone and its receptor during fetal mouse development

1980 ◽  
Vol 77 (5) ◽  
pp. 2782-2785 ◽  
Author(s):  
E. Nexo ◽  
M. D. Hollenberg ◽  
A. Figueroa ◽  
R. M. Pratt
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Mouse Development ◽  
Fetal Mouse ◽  
Epidermal Growth

Epidermal growth factor receptor (EGFR) involvement in successful growth hormone (GH) signaling in GH transduction defect

2017 ◽  
Vol 30 (2) ◽  
Author(s):  
Eirini Kostopoulou ◽  
Andrea Paola Rojas-Gil ◽  
Alexia Karvela ◽  
Bessie E. Spiliotis
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cellular Localization ◽  
Growth Hormone Receptor ◽  
Egf Receptor ◽  
Growth Factor Receptor ◽  
Physical Contact ◽  
Stat3 Phosphorylation ◽  
Epidermal Growth

AbstractBackground:Growth hormone (GH) transduction defect (GHTD) is a growth disorder with impaired signal transducer and activator of transcription 3 (STAT3) phosphorylation mediated by overexpression of cytokine-inducible SH2-containing protein (CIS), which causes increased growth hormone receptor (GHR) degradation. This study investigated the role of epidermal growth factor (EGF) in the restoration of normal GH signaling in GHTD.Methods:Protein expression, cellular localization and physical contact of proteins of the GH and EGF signaling pathways were studied by Western immunoblotting, immunofluorescence and co-immunoprecipitation, respectively. These were performed in fibroblasts of one GHTD patient (P) and one control child (C) at the basal state and after induction with human GH (hGH) 200 μg/L (GH200), either with or without silencing of CIS mRNA, and after induction with hGH 1000 μg/L (GH1000) or 50 ng/mL EGF.Results:The membrane availability of the EGF receptor (EGFR) and the activated EGFR (pEGFR) was increased in P only after simultaneous GH200 and silencing of CIS mRNA or with GH1000, whereas this occurred in C after GH200 alone. After EGF induction, the membrane localization of GHR, STAT3 and that of EGFR were increased in P more than in C.Conclusions:In conclusion, in GHTD, the EGFR seems to participate in successful GH signaling, but induction of GHTD fibroblasts with a higher dose of hGH is needed. The EGF/EGFR pathway, in contrast to the GH/GHR pathway, seems to function normally in P and is more primed compared to C. The involvement of the EGFR in successful GH signaling may explain the catch-up growth seen in the Ps when exogenous hGH is administered.

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