Cellular and Molecular Mechanisms of Gastric Ulcer Healing. Is the Quality of Mucosal Scar Affected by Treatment?

Tarnawski, Andrzej S.; Tanoue, Kazuo; Santos, Alicia M; Sarfeh, I. James

doi:10.3109/00365529509090261

Cited by 51 publications

(42 citation statements)

References 14 publications

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“…EGF-related peptides have been shown to prevent druginduced damage to the stomach, and to accelerate healing of gastric mucosal ulcerations (17,18), suggesting that EGF ligands play a major role in maintaining gastric mucosal integrity (26,27,48,49). In particular, HB-EGF recently has been demonstrated to be expressed in the normal human gastric mucosa (50), and to be upregulated after acute injury to the rat stomach (51) or kidney (52).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori upregulates expression of epidermal growth factor-related peptides, but inhibits their proliferative effect in MKN 28 gastric mucosal cells.

et al. 1998

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Acute exposure to Helicobacter pylori causes cell damage and impairs the processes of cell migration and proliferation in cultured gastric mucosal cells in vitro. EGF-related growth factors play a major role in protecting gastric mucosa against injury, and are involved in the process of gastric mucosal healing. We therefore studied the acute effect of H. pylori on expression of EGF-related growth factors and the proliferative response to these factors in gastric mucosal cells (MKN 28) derived from gastric adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori upregulates expression of epidermal growth factor-related peptides, but inhibits their proliferative effect in MKN 28 gastric mucosal cells.

et al. 1998

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“…The luminal aggressive factors (HCl secretion and pepsin) delay the ulcer healing. Inhibition of these factors by acid inhibitory drugs (H 2 blockers and proton pump inhibitors) is one of the major components of current peptic ulcer therapy (Tarnawski et al, 1995 andRobinson, 2004). Previous studies reported an antiacid action of the AEP (Freitas et al, 2004), which could contribute for the healing process that this extract presented.…”

Section: Resultsmentioning

confidence: 99%

Effects of Pfaffia glomerata (Spreng) pedersen aqueous extract on healing acetic acid-induced ulcers

Freitas

Baggio

Araújo

et al. 2008

Braz. arch. biol. technol.

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“…The role of EGFR in mediating biological properties of Sucralfate was described by Tarnawski et al (30). Recently it was demonstrated that EGFR also induces angiogenesis in murine skin carcinomas and other neoplasms, suggesting the ability ofEGFR to accelerate blood vessel formation during wound healing (12).…”

Section: Discussionmentioning

confidence: 99%

Sucralfate Modulates uPAR and EGFR Expression in an Experimental Rat Model of Cervicitis

Mannari¹,

Santi²,

Migliori³

et al. 2008

Int J Immunopathol Pharmacol

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Sucralfate is a drug used in the treatment of gastric and duodenal ulcer; it is cytoprotective and able to increase the bioavailability of several growth factors, modulating the wound healing process. In this study we tested the possible therapeutic effect of Sucralfate in the treatment of ulcerative lesion occurring in uterine cervix; to investigate such effect we used an experimental rat model of cervicitis in which the uPAR and EGFR expression were evaluated. Cervicitis was induced in wild and ovariectomized wistar female rats by an acetic acid-soaked tampon. The animals were divided into two main groups (4 and 7 days) and Sucralfate was administered topically until the day they were sacrificed. In order to distinguish physiological and drug-induced healing, quantitative and qualitative uPAR and EGFR expression were evaluated by using Western Blot and Immunohistochemistry techniques. Western Blot analysis demonstrated an increased expression of both receptors after 4 days from wounding in wild and ovariectomized animals. In particular in ovariectomized animals the expression of uPAR and EGFR increased after 4 days while it reduced following the administration of Sucralfate. In wild rats the same was observed for uPAR expression, while EGFR was different; in fact, its expression increased significantly at day 4 in the animals treated with the drug and only at day 7 in those untreated. Immunohistochemistry highlighted a noteworthy epithelial colocalization of EGFR and uPAR after 4 days in the animals treated with Sucralfate. We conclude that Sucralfate can promote the healing of ulcerative cervicitis and moreover, it reduces the normal healing time because of its modulatory property on uPAR and EGFR expression.

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Cellular and Molecular Mechanisms of Gastric Ulcer Healing. Is the Quality of Mucosal Scar Affected by Treatment?

Cited by 51 publications

References 14 publications

Helicobacter pylori upregulates expression of epidermal growth factor-related peptides, but inhibits their proliferative effect in MKN 28 gastric mucosal cells.

Helicobacter pylori upregulates expression of epidermal growth factor-related peptides, but inhibits their proliferative effect in MKN 28 gastric mucosal cells.

Effects of Pfaffia glomerata (Spreng) pedersen aqueous extract on healing acetic acid-induced ulcers

Sucralfate Modulates uPAR and EGFR Expression in an Experimental Rat Model of Cervicitis

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