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ZFP36L1在角质形成细胞中受生长因子和细胞因子调控,并影响其血管内皮生长因子(VEGF)的产生。

ZFP36L1 is regulated by growth factors and cytokines in keratinocytes and influences their VEGF production.

作者信息

Hacker Christine, Valchanova Ralitsa, Adams Stephanie, Munz Barbara

机构信息

Institute of Physiology, Charité - University Medicine Berlin, Arnimallee 22, D-14195, Berlin, Germany.

出版信息

Growth Factors. 2010 Jun;28(3):178-90. doi: 10.3109/08977190903578660.

Abstract

Keratinocyte-derived growth factors and cytokines play an important role in epidermal homeostasis and particularly in cutaneous wound repair. Thus, we analyzed a potential role of the ZFP36/tristetraprolin family of zinc finger proteins, which are targets of these factors, but also regulate their production, in keratinocytes. We show that expression of ZFP36, ZFP36L1, and ZFP36L2 is induced by a broad variety of growth factors and cytokines, and by scratch wounding. Since ZFP36L1 is a modulator of vascular endothelium growth factor (VEGF) mRNA stability, we subsequently used siRNA technology to inhibit ZFP36L1 gene expression. Notably, this treatment resulted in prolonged maintenance of elevated VEGF levels in HaCaT keratinocytes upon epidermal growth factor stimulation of these cells. Taken together, our results suggest an important role of ZFP36L1 in wound healing.

摘要

角质形成细胞衍生的生长因子和细胞因子在表皮稳态尤其是皮肤伤口修复中发挥着重要作用。因此,我们分析了锌指蛋白ZFP36/三基序蛋白家族在角质形成细胞中的潜在作用,该家族是这些因子的靶点,同时也调节它们的产生。我们发现,ZFP36、ZFP36L1和ZFP36L2的表达可由多种生长因子、细胞因子以及划痕损伤诱导。由于ZFP36L1是血管内皮生长因子(VEGF)mRNA稳定性的调节因子,我们随后使用小干扰RNA(siRNA)技术抑制ZFP36L1基因表达。值得注意的是,在表皮生长因子刺激HaCaT角质形成细胞后,这种处理导致VEGF水平升高的持续时间延长。综上所述,我们的结果表明ZFP36L1在伤口愈合中起重要作用。

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