Key roles for transforming growth factor beta in melanocyte stem cell maintenance.
Key roles for transforming growth factor beta in melanocyte stem cell maintenance.
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DOI：
10.1016/j.stem.2009.12.010
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发表时间：
2010-02-05
期刊：
影响因子：
23.9
通讯作者：
Fisher DE
中科院分区：
文献类型：
--
作者：
Nishimura EK;Suzuki M;Igras V;Du J;Lonning S;Miyachi Y;Roes J;Beermann F;Fisher DE
毛囊凸起区域的黑素细胞干细胞负责头发的色素沉着，它们的缺陷导致头发变白。本文描述了黑素细胞干细胞进入静止状态的过程，并表明小生境衍生的转化生长因子β (TGF-β)信号在这一过程中发挥了重要作用。在体外，TGF-β不仅诱导可逆的细胞周期阻滞，还通过下调MITF（黑素细胞分化的主要转录调控因子）及其下游的致黑基因，促进黑素细胞不成熟。在体内，当黑素细胞干细胞在毛发周期中重新进入静止的非循环状态时，TGF-β信号被激活，这一过程需要Bcl2来维持细胞存活。此外，黑素细胞谱系中靶向TGF-β II型受体（TGFbRII）缺乏导致黑素细胞干细胞不成熟的不完全维持，并导致轻度头发变白。这些数据表明，TGF-β信号通路是调控黑素细胞干细胞不成熟和静止的关键生态因子之一。
Melanocyte stem cells in the bulge area of hair follicles are responsible for hair pigmentation, and defects in them cause hair graying. Here we describe the process of melanocyte stem cell entry into the quiescent state and show that niche-derived transforming growth factor β (TGF-β) signaling plays important roles in this process. In vitro, TGF-β not only induces reversible cell cycle arrest, but also promotes melanocyte immaturity by downregulating MITF, the master transcriptional regulator of melanocyte differentiation, and its downstream melanogenic genes. In vivo, TGF-β signaling is activated in melanocyte stem cells when they reenter the quiescent noncycling state during the hair cycle and this process requires Bcl2 for cell survival. Furthermore, targeted TGF-β type II receptor (TGFbRII) deficiency in the melanocyte lineage causes incomplete maintenance of melanocyte stem cell immaturity and results in mild hair graying. These data demonstrate that the TGF-β signaling pathway is one of the key niche factors that regulate melanocyte stem cell immaturity and quiescence.
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