首页> 外文期刊>Kobe journal of medical sciences >Prostaglandin E2 Regulates the Expression of Basic Fibroblast Growth Factor Messenger RNA in Normal Human Fibroblasts
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Prostaglandin E2 Regulates the Expression of Basic Fibroblast Growth Factor Messenger RNA in Normal Human Fibroblasts

机译:前列腺素E2调节正常人成纤维细胞中碱性成纤维细胞生长因子信使RNA的表达。

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摘要

Prostaglandin E2 (PGE2) has been reported to control angiogenesis and play an important role in wound healing in soft tissues, although the precise mechanism is still unknown. Since basic fibroblast growth factor (bFGF) has been reported to generate neovascularization, PGE2 and bFGF might work closely, or one might control the expression of the other. In this study, we demonstrate that PGE2 enhances the expression of bFGF in normal human fibroblasts, and that calcium ionophore, A23187, and adenylate cyclase activator, forskolin, also enhances the expression bFGF mRNA. These results suggest that enhancement of bFGF mRNA stimulated by PGE2 is mainly controlled through EP1 or EP2 and EP4 receptor. In conclusion, our findings suggest that the mechanism of PGE2-induced angiogenesis and wound hearing in soft tissue could be mediated by bFGF through EP1 or EP2 and EP4 receptor.
机译:据报道,前列腺素E2(PGE2)可控制血管生成并在软组织的伤口愈合中起重要作用,尽管其确切机制尚不清楚。由于已报道碱性成纤维细胞生长因子(bFGF)产生新血管形成,因此PGE2和bFGF可能紧密起作用,或者一个可能控制另一个的表达。在这项研究中,我们证明PGE2增强正常人成纤维细胞中bFGF的表达,钙离子载体A23187和腺苷酸环化酶激活剂forskolin也增强bFGF mRNA的表达。这些结果表明,PGE2刺激的bFGF mRNA的增强主要通过EP1或EP2和EP4受体来控制。总之,我们的研究结果表明,bFGF可通过EP1或EP2和EP4受体介导PGE2诱导的软组织血管生成和伤口听力的机制。

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