Experimental and Clinical Studies on Epidermal Growth Factor for Gastric Mucosal Protection and Healing of Gastric Ulcers

Itoh, Makoto; Joh, Takashi; Imai, Seiji; Miyamoto, Tadahisa; Matsusako, Kei; Iwai, Akira; Katsumi, Kohei; Endo, Kazuo; Gotō, Kazuo; Takeuchi, Toshihiko

doi:10.1097/00004836-198812001-00003

Cited by 37 publications

(16 citation statements)

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“…Others have investigated motility (38) and chemotaxis ( 19) of individual cells. Previous attempts to model sheet migration have generally involved the radial migration ofcells from tissue explants (39)(40)(41) or the creation ofwounds in cell monolayers (42,43) or intact tissues (8,(13)(14)(15)(16)(17)43). Studies ofintact tissue or tissue explants may be difficult to control while cell injury occurring in wounding may release intracellular bioactive agents which confuse the assay (42).…”

Section: Discussionmentioning

confidence: 99%

“…EGF is present throughout the gastrointestinal tract (9)(10)(11) together with the related peptide TGFa which appears to activate the same receptor ( 12). Furthermore, the mucosal injury produced by peptic ulcer disease or Crohn's disease induces gastrointestinal stem cells to differentiate into an EGF-secreting lineage (10) while peptic ulcer disease may be associated with increased salivary secretion of EGF ( 13). Both EGF and EGF receptor immunoreactivity have been reported to be increased within the oxyntic mucosa of rats in which ischemic gastric ulceration had been induced ( 14).…”

Section: Introductionmentioning

confidence: 99%

“…Both EGF and EGF receptor immunoreactivity have been reported to be increased within the oxyntic mucosa of rats in which ischemic gastric ulceration had been induced ( 14). Long known to potentiate epithelial healing in the skin ( 15,16), EGF has, in addition, been reported to promote gastrointestinal mucosal wound healing in animal models ( 13,17). The mechanism of the EGF effect in the gut is unclear, and has previously been attributed to mitogenicity ( 17) or to "cytoprotection."…”

Section: Introductionmentioning

confidence: 99%

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Human enterocyte (Caco-2) migration is modulated in vitro by extracellular matrix composition and epidermal growth factor.

Basson¹,

Modlin²,

Madri³

1992

J. Clin. Invest.

181

131

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The modulation of enterocyte sheet migration was studied using Caco-2 cells, a well-differentiated human colonic cell line. Although Caco-2 cells attached and spread equivalently over collagen types I, III, IV, and V and laminin, migration over laminin was significantly slower than migration over the collagen types. Fibronectin was a poor substrate for attachment, spreading, and migration. Epidermal growth factor (EGF) stimulated migration over laminin but did not alter Caco-2 migration over collagen or fibronectin. This effect was independent of cell proliferation, which was stimulated equivalently on both laminin and collagen I. Expression and organization of cell surface receptors for matrix (integrins) were studied using antibodies specific for f and a integrin subunits. Integrin surface expression was assessed by immunoprecipitation of surface l25i dinated control and EGF-treated cells. fi1 surface pools did not change substantially in any condition studied. al subunit pools were decreased after EGF treatment on collagen I but al pools increased after EGF treatment on laminin. Surface pools of a2 subunits were increased following EGF treatment whether cells were cultured on laminin or collagen I. However, traditional immunofluorescent and laser confocal imaging demonstrated substantial differences in the character of a2 subunit organization between collagen and laminin in the migrating cell front. Furthermore, a functional antibody to the a2 subunit inhibited EGF stimulation of migration over laminin without substantial effects on basal migration over laminin or collagen I. Thus, EGF appears to exert a matrix-specific effect on enterocyte migration by modulation of integrin expression and organization. (J. Clin. Invest. 1992. 90:15-23.)

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Human enterocyte (Caco-2) migration is modulated in vitro by extracellular matrix composition and epidermal growth factor.

Basson¹,

Modlin²,

Madri³

1992

J. Clin. Invest.

181

131

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“…• Somam-se às evidências da atuação do EGF na integridade da mucosa do trato digestivo os estudos que administraram EGF, seja tópico 9,22 , seja sistêmico 14 • Estudos populacionais recentes mostram que mais de 30% da população geral apresenta sintomas ocasionais dispépticos e laringofaríngeos associados ao refluxo gastroesofágico e que em até 40% destes indivíduos o exame endoscópico da mucosa digestiva é normal 19 . Estes achados chamam a atenção para o comportamento silencioso da DRGE, mas também nos fazem inferir que possivelmente haja mais fatores envolvidos na fiosiopatologia da DRGE do que simplesmente o refluxo do conteúdo gastroduodenal, seja ácido ou alcalino.…”

Section: Discussionunclassified

“…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 .…”

Section: Introductionunclassified

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

Eckley

Costa

2003

Rev. Bras. Otorrinolaringol.

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Int rodução: A Doença do Refluxo Gastroesofágico (DRGE), chegando até a faringe e laringe, pode cursar com intensa inflamação local e rica sintomatologia (Refluxo Laringofaríngeo -RLF). Os estudos atuais não foram capazes de provar que o ácido refluído é o causador das alterações visualizadas na laringite crônica. O Fator de Crescimento Epidérmico (EGF) é um polipeptídeo produzido pelas glândulas salivares, sendo implicado na indução do crescimento epitelial, na inibição da secreção gástrica e na aceleração da cicatrização. Deficiência salivar deste fator foi encontrada na esofagite de refluxo, mas não há relatos sobre a concentração salivar de EGF em indivíduos com RLF. Objetivo: Determinar a concentração salivar do EGF em indivíduos com RLF. Forma de estudo: Caso controle. Casuística e Método: A concentração salivar de EGF de 39 indivíduos com RLF e 20 controles normais foi estudada pela técnica de ELISA. O RLF foi diagnosticado por história e exame videolaringoscópico característicos. Os 39 pacientes com RLF foram estratificados de acordo com os achados de endoscopia digestiva (com ou sem esofagite associada) e de acordo com a intensidade da laringite crônica. Foram, também, submetidos a manometria esofágica e pH-metria esofágica de 24 horas com dois canais. Resultados: Constatou-se uma concentração de EGF significativamente menor nos indivíduos com RLF quando comparados aos controles normais (p=0,002). Não houve diferença estatisticamente significante na concentração salivar de EGF entre os indivíduos com RLF, nem em relação à presença de esofagite, nem quanto à intensidade da laringite. Conclusões: Este estudo sugere que uma deficiência na concentração salivar do Fator de Crescimento Epidérmico pode estar associada à patogenia da DRGE, e que este polipeptídeo poderia ser um co-fator na gênese do RLF. Claudia

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Somatostatin Analogue Inhibits Intestinal Regeneration

1993

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Somatostatin analogue octreotide inhibits intestinal absorption and motility but its effect on epithelial cell migration and proliferation remains unclear. Our aim was to determine the effect of octreotide on parameters of intestinal regeneration, including epidermal growth factor (EGF)-induced changes. Thirty rabbits had full-thickness ileal defects patched with cecal serosa surface. Group 1 were controls. Groups 2 and 3 received 100 micrograms and 1000 micrograms, respectively, of subcutaneous octreotide daily. Group 4 received EGF at 1.5 micrograms/kg per hour via subcutaneous miniosmotic pump, and group 5 received both octreotide (1000 micrograms/d) and EGF (1.5 micrograms/kg per hour). Octreotide at 100 micrograms/d did not inhibit epithelial cell migration or proliferation at 7 days. Octreotide at 1000 micrograms/d inhibited normal but not EGF-stimulated cell migration. Octreotide decreased EGF-stimulated but not normal proliferation. Octreotide impairs epithelial cell migration in a dose-dependent manner. Octreotide inhibits EGF-stimulated proliferative activity but not EGF-stimulated migration. Prolonged administration of octreotide may adversely affect normal and adaptive intestinal regeneration by both direct and indirect effects.

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Experimental and Clinical Studies on Epidermal Growth Factor for Gastric Mucosal Protection and Healing of Gastric Ulcers

Cited by 37 publications

References 0 publications

Human enterocyte (Caco-2) migration is modulated in vitro by extracellular matrix composition and epidermal growth factor.

Human enterocyte (Caco-2) migration is modulated in vitro by extracellular matrix composition and epidermal growth factor.

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

Somatostatin Analogue Inhibits Intestinal Regeneration

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