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Dev Cell:前列腺素浓度影响干细胞分化方向

来源:生物谷 2014-02-16 00:08

2014年2月16日 讯 /生物谷BIOON/ --哈佛干细胞学家揭示了在发育过程中干细胞是分化为肝脏细胞还是胰脏细胞的分子机制。科学家发现细胞命运是受前列腺素E2(prostaglandin E2)的浓度影响的。该研究发表在近期的Developmental Cell杂志上,对在实验室环境中构建肝脏和胰脏和未来的细胞治疗有重要意义。

科学家在斑马鱼胚胎中发现在干细胞分化为内在的区域前列腺素E2存在浓度梯度。该文章的第一作者Sahar Nissim博士发现将要分化为肝脏和胰脏的干细胞表面存在特殊受体,该受体能够检测前列腺素E2的量,并定向分化为不同类型的细胞。

该文章的通讯作者Wolfram Goessling博士称,周围前列腺素E2浓度高的干细胞变成了肝脏细胞,周围前列腺素E2浓度低的干细胞最终成为胰脏细胞。我们首次证明了前列腺素能够决定细胞命运。

揭示了前列腺素E2对肝脏和胰脏发育的影响,科学家进一步打算将其用于诱导IPS细胞转化为肝脏或胰脏。科学家预测该研究将给需要肝脏移植的病人带来福音。(生物谷Bioon.com)

doi:10.1016/j.devcel.2014.01.006

Prostaglandin E2 Regulates Liver versus Pancreas Cell-Fate Decisions and Endodermal Outgrowth

Sahar Nissim, Richard I. Sherwood, Julia Wucherpfennig, Diane Saunders, James M. Harris, Virginie Esain, Kelli J. Carroll, Gregory M. Frechette, Andrew J. Kim, Katie L. Hwang, Claire C. Cutting, Susanna Elledge, Trista E. North, Wolfram Goessling

The liver and pancreas arise from common endodermal progenitors. How these distinct cell fates are specified is poorly understood. Here we describe prostaglandin E2 (PGE2) as a regulator of endodermal fate specification during development. Modulating PGE2 activity has opposing effects on liver versus pancreas specification in zebrafish embryos as well as mouse endodermal progenitors. The PGE2 synthetic enzyme cox2a and receptor ep2a are patterned such that cells closest to PGE2 synthesis acquire a liver fate, whereas more distant cells acquire a pancreas fate. PGE2 interacts with the bmp2b pathway to regulate fate specification. At later stages of development, PGE2 acting via the ep4a receptor promotes outgrowth of both the liver and pancreas. PGE2 remains important for adult organ growth, as it modulates liver regeneration. This work provides in vivo evidence that PGE2 may act as a morphogen to regulate cell-fate decisions and outgrowth of the embryonic endodermal anlagen.

 

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