Distribution and release of epidermal growth factor in man.

Abstract

SUMMARY Epidermal growth factor (EGF) is localised in man to salivary and Brunner's glands. It is present in large concentrations in saliva and duodenal contents but the mechanisms of its release have been little studied. This study carried out on four groups of healthy subjects was designed to determine the distribution and the release of immunoreactive EGF (IR-EGF) in salivary, gastric, duodenal, and pancreatic secretions. Under basal conditions, the concentrations of IR-EGF in salivary, gastric, duodenal and pancreatic secretions were; 2.7 (0.4), 0.42 (0.12), 21 (5) and 8.5 (1.2) ng/ml, respectively. Chewing of Parafilm* significantly increased salivary but not gastric or duodenal EGF output while atropinisation led to the reduction in basal salivary and duodenal EGF output without affecting the increment in EGF release induced by chewing. Cigarette smoking caused a marked reduction in basal salivary and duodenal EGF output. Infusion of pentagastrin increased salivary and duodenal EGF output and this was blocked by the addition of somatostatin. Injection of secretin lead to an increase in pancreatic output of EGF. We conclude that in man the major sources of EGF are salivary glands, duodenum, and pancreas and that the release of EGF remains under neurohormonal control.Epidermal growth factor (EGF) originally isolated by Cohen' from the mouse submaxillary glands is a 53 amino acid peptide structurally resembling urogastrone, another peptide isolated from urine.' Urogastrone was discovered after the observation that the extracts of urine from pregnant women had beneficial effect on healing of chronic ulcers in MannWilliamson dogs.3Studies on animals showed that EGF, like urogastrone, displays many kinds of biological effects including stimulation of proliferation and differentiation of epithelial and non-epithelial tissues"4, stimulation of DNA synthesis4 through increasing ornithine decarboxylase activity,' protection of the gastroduodenal mucosa against various irritants, enhancement of healing of chronic gastroduodenal ulceration`and inhibition of gastric acid secretion." Epidermal growth factor has been reported to be Address for correspondenIcice: Prof D)r S J Konturek. Institute of lPhysiology.31-531 Kr,tkow ul. Grzegorzecka 16. Poilnd.

Insect tea attenuates hydrochloric acid and ethanol‑induced mice acute gastric injury

“…EGF stimulates cell growth, proliferation and differentiation by binding to EGFR, which is secreted by the salivary glands, Brunner's glands in the duodenum and pancreas (58). In the present study, insect tea treatment significantly increased the levels of EGF and EGFR in the gastric tissue of ulcer mice.…”

“…In the present study, insect tea treatment significantly increased the levels of EGF and EGFR in the gastric tissue of ulcer mice. Under normal physiological conditions, EGF inhibits gastric acid secretion, reducing the activity of gastric protease, promoting gastric epithelial cell proliferation and preventing ulcer formation (58,59). EGF also accelerates healing in gastric ulcers by promoting cell DNA synthesis in the gastric mucosa (59,60).…”

Estudo da concentração salivar do fator de crescimento epidérmico em indivíduos com laringite crônica por refluxo laringofaríngeo

“…Entre os fatores orgânicos biologicamente ativos produzidos pelas glândulas salivares, o Fator de Crescimento Epidérmico (EGF), devido ao seu poder de estimular a síntese celular de DNA, mostrou ser aquele que mais diretamente está associado à rápida regeneração dos epitélios oral e digestivo, após as agressões [10][11][12]15,21 . Estudos quantitativos e qualitativos da ação biológica dos polipeptídeos salivares como as prostaglandinas (PGE), o fator de transformação do crescimento (TGF) com suas subfrações alfa e beta e o fator de crescimento epidérmico (EGF) mostraram que apesar de todos atuarem direta ou indiretamente na proteção do epitélio digestivo, o mais ativo destes polipeptídeos, tanto pela sua concentração salivar quanto pela sua ação biológica, é o EGF 11 .…”

“…Há, no entanto, diversos estudos descrevendo a diminuição dos elementos orgânicos como o Fator de Crescimento Epidérmico (EGF), as Prostaglandinas (PG), o Fator de Transformação do Crescimento (em especial sua sub-fração, o TGF2 alfa), entre outros, em pacientes com esofagite de refluxo e doença dispéptica 6,[9][10][11][12][13] . Outros estudos demonstram recuperação mais precoce de lesões da mucosa gástrica e esofágica após a infusão endovenosa do EGF, sugerindo uma atividade importante deste polipeptídeo na cicatrização e regeneração epitelial 14,15 .…”

Cigarette Smoke Increases Apoptosis in the Gastric Mucosa: Role of Epidermal Growth Factor

“…It has been reported that depletion of EGF or application of monoclonal antibody against EGF receptor could induce apoptosis in vitro [13, 14], and the EGF protects colonic epithelial cells from the induction of apoptosis in the absence of serum over 24 h [15]. Clinical studies have indicated that smokers have a low level of EGF in the saliva [16]. Therefore, we wanted to discover whether passive cigarette smoke exposure, using an established animal model [17], would cause any adverse effects on cell apoptosis in the gastric mucosa.…”