Connective Tissue Growth Factor in Indomethacin-Induced Rat Gastric Ulcer
| Autor: | K. Inkinen, Henrik Wolff, Marko Lempinen, J. Ahonen |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Male
medicine.medical_specialty Angiogenesis medicine.medical_treatment Indomethacin Gene Expression Connective tissue In situ hybridization Biology Immediate-Early Proteins Transforming Growth Factor beta Internal medicine medicine Animals RNA Messenger Stomach Ulcer Northern blot In Situ Hybridization integumentary system Growth factor Anti-Inflammatory Agents Non-Steroidal Connective Tissue Growth Factor Rats Inbred Strains Rats CTGF Collagen Type III Endocrinology medicine.anatomical_structure Intercellular Signaling Peptides and Proteins Surgery Wound healing Transforming growth factor |
| Zdroj: | European Surgical Research. 34:232-238 |
| ISSN: | 1421-9921 0014-312X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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