2002European Surgical ResearchRequires access

Connective Tissue Growth Factor in Indomethacin-Induced Rat Gastric Ulcer

Marko Lempinen, Kaija Inkinen, Henrik Wolff, J. Ahonen

Open publisher page 8 citations

Abstract

The healing of gastric ulcers requires not only the complete epithelial covering but also the restitution of connective tissue. Transforming growth factor-beta (TGF-beta) and its downstream mediator, connective tissue growth factor (CTGF), are potent stimulators for connective tissue formation during wound healing. The expression of TGF-beta, CTGF and type III collagen mRNA in indomethacin-induced gastric ulcers in rat, was investigated by Northern blot analysis. We also examined the localization of CTGF producing cells by in situ hybridization. Northern blot analysis showed expression of TGF-beta mRNA on days 1 and 3 after indomethacin administration, expression of CTGF mRNA on days 1, 3 and 7 and type III collagen mRNA expression on days 1, 3, 7 and 12, respectively. Control animals showed no expression of TGF-beta, CTGF or type III collagen mRNA. In situ hybridization showed CTGF mRNA positive cells on days 1, 3 and 7 after ulcer induction in fibroblast-like cells and in some of the blood vessels. Thus our findings indicate that growth factor CTGF, together with TGF-beta, participates in gastric ulcer healing by regulating connective tissue formation and angiogenesis. These results are compatible with the role of CTGF as a downstream mediator of TGF-beta effects.

About this research paper

What this paper is about

The healing of gastric ulcers requires not only the complete epithelial covering but also the restitution of connective tissue. Transforming growth factor-beta (TGF-beta) and its downstream mediator, connective tissue growth factor (CTGF), are potent stimulators for connective tissue formation during wound healing. The expression of TGF-beta, CTGF and type III collagen mRNA in indomethacin-induced gastric ulcers in rat, was investigated by Northern blot analysis. We also examined the localization of CTGF producing cells by in situ hybridization. Northern blot analysis showed expression of TGF-beta mRNA on days 1 and 3 after indomethacin administration, expression of CTGF mRNA on days 1, 3 and 7 and type III collagen mRNA expression on days 1, 3, 7 and 12, respectively. Control animals showed no expression of TGF-beta, CTGF or type III collagen mRNA. In situ hybridization showed CTGF mRNA positive cells on days 1, 3 and 7 after ulcer induction in fibroblast-like cells and in some of the blood vessels. Thus our findings indicate that growth factor CTGF, together with TGF-beta, participates in gastric ulcer healing by regulating connective tissue formation and angiogenesis. These results are compatible with the role of CTGF as a downstream mediator of TGF-beta effects.

Why it matters

OpenAlex reports 8 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

The healing of gastric ulcers requires not only the complete epithelial covering but also the restitution of connective tissue. Transforming growth factor-beta (TGF-beta) and its downstream mediator, connective tissue growth factor (CTGF), are potent stimulators for connective tissue formation during wound healing. The expression of TGF-beta, CTGF and type III collagen mRNA in indomethacin-induced gastric ulcers in rat, was investigated by Northern blot analysis. We also examined the localization of CTGF producing cells by in situ hybridization. Northern blot analysis showed expression of TGF-beta mRNA on days 1 and 3 after indomethacin administration, expression of CTGF mRNA on days 1, 3 and 7 and type III collagen mRNA expression on days 1, 3, 7 and 12, respectively. Control animals showed no expression of TGF-beta, CTGF or type III collagen mRNA. In situ hybridization showed CTGF mRNA positive cells on days 1, 3 and 7 after ulcer induction in fibroblast-like cells and in some of the blood vessels. Thus our findings indicate that growth factor CTGF, together with TGF-beta, participates in gastric ulcer healing by regulating connective tissue formation and angiogenesis. These results are compatible with the role of CTGF as a downstream mediator of TGF-beta effects.

Key concepts: CTGF, Connective tissue, Growth factor, In situ hybridization, Wound healing, Northern blot, Transforming growth factor beta, Transforming growth factor

Related papers

Back to paper searchBrowse research topicsOriginal source
Connective Tissue Growth Factor in Indomethacin-Induced Rat Gastric Ulcer — Research Paper | ScholarLens