FGF2 regulates melanocytes viability through the STAT3-transactivated PAX3 transcription.

FGF2 regulates melanocytes viability through the STAT3-transactivated PAX3 transcription.
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DOI:
10.1038/cdd.2011.132
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发表时间:
2012-04
影响因子:
12.4
通讯作者:
--
中科院分区:
生物学1区
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--
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PAX 3(配对框3)已知通过调节小眼症相关转录因子转录在黑素细胞发育中具有重要作用。我们发现PAX 3的转录活性可以通过色素细胞中的FGF 2(碱性成纤维细胞生长因子)-STAT 3(信号转导子和转录激活子3)信号转导来调节。为了研究其在体内的功能,我们已经建立了一个转基因小鼠模型,表达PAX 3酪氨酸酶启动子驱动的组织特异性的方式。这些动物在表皮上表现出色素沉着,明显的是它们耳朵和尾巴的皮肤颜色。我们发现,黑色素细胞数量和黑色素合成的增加都是导致皮肤颜色变深的原因。总之,我们的研究描绘了黑素细胞谱系中的一种新途径,将FGF 2-STAT 3信号传导与PAX 3转录增加联系起来。此外,我们的研究结果表明,这一途径可能有助于调节黑素细胞的数量和黑素水平,从而提供了一种替代的策略,以诱导色素沉着。
PAX3 (paired box 3) is known to have an important role in melanocyte development through modulation of microphthalmia-associated transcription factor transcription. Here we found that PAX3 transcriptional activity could be regulated through FGF2 (basic fibroblast growth factor)-STAT3 (signal transducer and activator of transcription 3) signaling in the pigment cells. To study its function in vivo, we have generated a transgenic mouse model expressing PAX3 driven by tyrosinase promoter in a tissue-specific fashion. These animals exhibit hyperpigmentation in the epidermis, evident in the skin color of their ears and tails. We showed that the darker skin color results from both increased melanocyte numbers and melanin synthesis. Together, our study delineated a novel pathway in the melanocyte lineage, linking FGF2-STAT3 signaling to increased PAX3 transcription. Moreover, our results suggest that this pathway might contribute to the regulation of melanocyte numbers and melanin levels, and thereby provide an alternative strategy to induce pigmentation.
DOI: 10.1084/jem.20030077
发表时间: 2003-11-17
期刊: The Journal of experimental medicine
影响因子: --
作者:
Kano A;Wolfgang MJ;Gao Q;Jacoby J;Chai GX;Hansen W;Iwamoto Y;Pober JS;Flavell RA;Fu XY
通讯作者: Fu XY
DOI: 10.1073/pnas.90.2.532
发表时间: 1993-01-15
影响因子: 11.1
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影响因子: 3.5
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发表时间: 2003-11-15
影响因子: 4.2
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DOI: 10.1111/j.1600-0749.1996.tb00089.x
发表时间: 1996-04-01
期刊: PIGMENT CELL RESEARCH
影响因子: --
作者:
Horikawa, T;Norris, DA;Morelli, JG
通讯作者: Morelli, JG