Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats

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Standard

Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats. / Juhl, C O; Vinter-Jensen, Lars; Poulsen, Steen Seier; Orntoft, T F; Dajani, E Z.

I: Digestive Diseases and Sciences, Bind 40, Nr. 12, 12.1995, s. 2717-23.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Juhl, CO, Vinter-Jensen, L, Poulsen, SS, Orntoft, TF & Dajani, EZ 1995, 'Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats', Digestive Diseases and Sciences, bind 40, nr. 12, s. 2717-23.

APA

Juhl, C. O., Vinter-Jensen, L., Poulsen, S. S., Orntoft, T. F., & Dajani, E. Z. (1995). Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats. Digestive Diseases and Sciences, 40(12), 2717-23.

Vancouver

Juhl CO, Vinter-Jensen L, Poulsen SS, Orntoft TF, Dajani EZ. Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats. Digestive Diseases and Sciences. 1995 dec.;40(12):2717-23.

Author

Juhl, C O ; Vinter-Jensen, Lars ; Poulsen, Steen Seier ; Orntoft, T F ; Dajani, E Z. / Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats. I: Digestive Diseases and Sciences. 1995 ; Bind 40, Nr. 12. s. 2717-23.

Bibtex

@article{b4fb07cc262b45e089d9ff833448a8d5,
title = "Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats",
abstract = "Epidermal growth factor (EGF) is an important factor for maintaining the esophageal functional integrity. Goettingen minipigs were treated with either placebo or subcutaneous EGF (30 micrograms/kg/day) for four weeks. Wistar rats were treated with either placebo or subcutaneous EGF (150 micrograms/kg/day) for four weeks. At sacrifice, esophageal samples were obtained for histology, immunochemistry, and lectin characterization. In pigs, the thickness of the esophageal epithelium was almost doubled in the EGF-treated animals. Characterization with lectins revealed a normal pattern of differentiation. Subcutaneously administered EGF was visualized on cells located basally in the esophageal epithelium. In rats, EGF-treatment increased the esophageal volume of the epithelium, the lamina propria of the mucosa, and the submucosa. In conclusion, systemic EGF challenge induces growth of the esophageal epithelium with an unaltered pattern of differentiation. This supports previous studies demonstrating a beneficial effects of systemic EGF-treatment on sclerotherapy-induced esophageal damage.",
keywords = "Animals, Cell Differentiation, Epidermal Growth Factor, Epithelium, Esophagus, Female, Hyperplasia, Lectins, Male, Rats, Rats, Wistar, Swine, Swine, Miniature, Time Factors",
author = "Juhl, {C O} and Lars Vinter-Jensen and Poulsen, {Steen Seier} and Orntoft, {T F} and Dajani, {E Z}",
year = "1995",
month = dec,
language = "English",
volume = "40",
pages = "2717--23",
journal = "Digestive Diseases and Sciences",
issn = "0163-2116",
publisher = "Springer",
number = "12",

}

RIS

TY - JOUR

T1 - Chronic treatment with epidermal growth factor causes esophageal epithelial hyperplasia in pigs and rats

AU - Juhl, C O

AU - Vinter-Jensen, Lars

AU - Poulsen, Steen Seier

AU - Orntoft, T F

AU - Dajani, E Z

PY - 1995/12

Y1 - 1995/12

N2 - Epidermal growth factor (EGF) is an important factor for maintaining the esophageal functional integrity. Goettingen minipigs were treated with either placebo or subcutaneous EGF (30 micrograms/kg/day) for four weeks. Wistar rats were treated with either placebo or subcutaneous EGF (150 micrograms/kg/day) for four weeks. At sacrifice, esophageal samples were obtained for histology, immunochemistry, and lectin characterization. In pigs, the thickness of the esophageal epithelium was almost doubled in the EGF-treated animals. Characterization with lectins revealed a normal pattern of differentiation. Subcutaneously administered EGF was visualized on cells located basally in the esophageal epithelium. In rats, EGF-treatment increased the esophageal volume of the epithelium, the lamina propria of the mucosa, and the submucosa. In conclusion, systemic EGF challenge induces growth of the esophageal epithelium with an unaltered pattern of differentiation. This supports previous studies demonstrating a beneficial effects of systemic EGF-treatment on sclerotherapy-induced esophageal damage.

AB - Epidermal growth factor (EGF) is an important factor for maintaining the esophageal functional integrity. Goettingen minipigs were treated with either placebo or subcutaneous EGF (30 micrograms/kg/day) for four weeks. Wistar rats were treated with either placebo or subcutaneous EGF (150 micrograms/kg/day) for four weeks. At sacrifice, esophageal samples were obtained for histology, immunochemistry, and lectin characterization. In pigs, the thickness of the esophageal epithelium was almost doubled in the EGF-treated animals. Characterization with lectins revealed a normal pattern of differentiation. Subcutaneously administered EGF was visualized on cells located basally in the esophageal epithelium. In rats, EGF-treatment increased the esophageal volume of the epithelium, the lamina propria of the mucosa, and the submucosa. In conclusion, systemic EGF challenge induces growth of the esophageal epithelium with an unaltered pattern of differentiation. This supports previous studies demonstrating a beneficial effects of systemic EGF-treatment on sclerotherapy-induced esophageal damage.

KW - Animals

KW - Cell Differentiation

KW - Epidermal Growth Factor

KW - Epithelium

KW - Esophagus

KW - Female

KW - Hyperplasia

KW - Lectins

KW - Male

KW - Rats

KW - Rats, Wistar

KW - Swine

KW - Swine, Miniature

KW - Time Factors

M3 - Journal article

C2 - 8536536

VL - 40

SP - 2717

EP - 2723

JO - Digestive Diseases and Sciences

JF - Digestive Diseases and Sciences

SN - 0163-2116

IS - 12

ER -

ID: 47487033