Oral administration of synthetic human urogastrone promotes healing of chronic duodenal ulcers in rats

Olsen, Peter Skov; Poulsen, Steen Seier; Therkelsen, Kim; Nexø, Ebba

doi:10.1016/0016-5085(86)90867-x

Cited by 87 publications

(10 citation statements)

References 30 publications

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“…15 For the assay, 60 μΐ of Standard or sample were placed in duplicate into consecutive wells of a coated microtitre plate. An 8 h incubation period at room temperature was started by adding 90 μΐ of an antibody mixture containing the monoclonal anti epidermal growth factor at a l: 90 000 dilution and the biotinylated rabbit anti epidermal growth factor at a l: 9000 dilution in assay buffer.…”

Section: Samples and Patient Collectivesmentioning

confidence: 99%

Gastric Ulcer is Accompanied by a Decrease of Epidermal Growth Factor in Gastric Juice and Saliva

Hansen

Müller²,

Sinha³

et al. 1989

Clinical Chemistry and Laboratory Medicine

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Nuinerous studies have indicated a role of epidermal growth factor in the maintenance of the gastrointestinal mucosa.In the present study epidermal growth factor concentrations in saliva and gastric juice of patients with gastric or duodenal ulcer or gastritis are compared with those of healthy controls. For this purpose a novel ELISA System has been developed and shown to be sensitive and specific.It is demonstrated that gastric juice and saliva of patients with gastric ulcer contain less epidermal growth factor than the samples of healthy controls (p < 0.01). Epidermal growth factor concentrations and Outputs (product of epidermal growth factor concentration and the volume secreted in 15 min) in the gastric juice of patients with duodenal ulcer do not differ frona those of healthy controls.

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Section: Samples and Patient Collectivesmentioning

confidence: 99%

Gastric Ulcer is Accompanied by a Decrease of Epidermal Growth Factor in Gastric Juice and Saliva

Hansen

Müller²,

Sinha³

et al. 1989

Clinical Chemistry and Laboratory Medicine

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“…Both EGF and TGF-a directly stimulate mucosal growth and inhibit gastric acid secretion, actions which protect the stomach against ulceration from excessive gastric acid secretion (14,26,41,50). EGF also stimulates gastrin gene transcription (24).…”

mentioning

confidence: 99%

A GC-rich element confers epidermal growth factor responsiveness to transcription from the gastrin promoter.

Merchant¹,

Demediuk²,

Brand³

1991

Mol. Cell. Biol.

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Epidermal growth factor (EGF) and transforming growth factor a are important determinants of mucosal integrity in the gastrointestinal tract, and they act both directly and indirectly to prevent ulceration in the stomach. Consistent with this physiological role, EGF stimulates transcription of gastrin, a peptide hormone which regulates gastric acid secretion and mucosal growth. EGF stimulation of gastrin transcription is mediated by a GC-rich gastrin EGF response element (gERE) (GGGGCGGGGTGGGGGG) which lies between -54 and -68 in the human gastrin promoter. The gERE sequence also confers weaker responsiveness to phorbol ester stimulation. The gERE sequence differs from previously described EGF response elements. The gERE DNA sequence specifically interacts with a GH4 DNA-binding protein distinct from previously described transcription factors (Egr-1 and AP2) which bind GC-rich sequences and mediate transcriptional activation by growth factors. Furthermore, the gERE element does not bind the Spl transcription factor even though the gERE sequence contains a high-affinity Spl-binding site (GGCGGG).

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“…Recent reports have indicated that many growth factors play an important role in the healing of gastrointestinal ulcers (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). In the present study, we examined the role of endogenous bFGF in the healing of gastric ulcers in duced by acetic acid in the rat and obtained the following results: 1) the content of bFGF in the ulcerated area in creased during the period of ulcer healing; 2) upon histo logical examination, many cells responding to anti-bFGF antiserum were seen in the ulcer bed 7 days after ulcer formation, and most of them were fibroblasts, macro phages and vascular endothelial cells; 3) ulcer healing was significantly inhibited by the administration of anti-bFGF monoclonal antibody 3H3; and 4) ulcer healing was obviously accelerated by the administration of TGP-580, recombinant human bFGF mutein CS23.…”

Section: Discussionmentioning

confidence: 99%

Role of Endogenous Basic Fibroblast Growth Factor in the Healing of Gastric Ulcers in Rats.

et al. 1997

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ABSTRACT-Recently, it has been pointed out that growth factors play an important role in the healing of gastrointestinal ulcers. In the present study, we examined the role of endogenous basic fibroblast growth factor (bFGF) in the healing of gastric ulcers in the rat. In male SD rats, gastric ulcers were induced in the antrum by injection of acetic acid. Time-dependent changes in the area and bFGF content in the ulcerated area and distribution of bFGF in the ulcerated mucosa were examined. Effects of bFGF mutein CS23 (TGP-580) and a monoclonal antibody for bFGF (MAb 3H3) on the healing of the gastric ulcers and angiogenesis in the ulcer bed were also examined. The content of bFGF in the ulcerated area increased with time as the ulcer healed and reached a maximum 7 days after ulcer formation. In the gastric ulcer bed, many cells such as fibroblasts and macrophages were positively stained immunohistochemically by anti-bFGF antiserum. MAb 3H3 (0.1 mg/rat/day, i.v.) inhibited angiogenesis in the ulcer bed and significantly delayed ulcer healing, while TGP-580 (0.001 -0.1 mg/kg x 2/day, p.o.) increased the number of microvessels in the ulcer bed and accelerated the healing. These results suggest that endogenous bFGF may play an important role in the healing of gastric ulcers in the rat and that the angiogenic properties of bFGF (TGP-580) may be involved in its effect on ulcer healing.

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Oral administration of synthetic human urogastrone promotes healing of chronic duodenal ulcers in rats

Cited by 87 publications

References 30 publications

Gastric Ulcer is Accompanied by a Decrease of Epidermal Growth Factor in Gastric Juice and Saliva

Gastric Ulcer is Accompanied by a Decrease of Epidermal Growth Factor in Gastric Juice and Saliva

A GC-rich element confers epidermal growth factor responsiveness to transcription from the gastrin promoter.

Role of Endogenous Basic Fibroblast Growth Factor in the Healing of Gastric Ulcers in Rats.

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