日本東京工業(yè)大學(xué)研究人員在新一期英國(guó)《自然》雜志上發(fā)表論文說(shuō),，他們通過(guò)向?qū)嶒?yàn)鼠的受精卵導(dǎo)入3個(gè)基因,，成功令其胚胎的中胚層分化成純粹的心肌細(xì)胞。
獲得這項(xiàng)成果的是東京工業(yè)大學(xué)的竹內(nèi)純等研究人員。他們將“Gata4”,、“Tbx5”和“Baf60C”3個(gè)基因?qū)胧芫诹斓膶?shí)驗(yàn)鼠受精卵中,，結(jié)果受精卵逐漸變成胚胎后，本該分化成手腳肌肉和胎兒羊膜的中胚層細(xì)胞分化生成了心肌細(xì)胞,。
向胚胎干細(xì)胞或誘導(dǎo)多能干細(xì)胞添加生理活性物質(zhì)等也能培養(yǎng)出心肌細(xì)胞,。但是，用這類方法培育出的心肌細(xì)胞往往混在多種細(xì)胞之中,，而這次研究人員培育出的心肌細(xì)胞完全沒有混雜別的細(xì)胞,。這項(xiàng)成果將有助于推動(dòng)心臟再生醫(yī)療研究以及解開心臟發(fā)育的機(jī)制。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 26 April 2009 | doi:10.1038/nature08039
Directed transdifferentiation of mouse mesoderm to heart tissue by defined factors
Jun K. Takeuchi1,2 & Benoit G. Bruneau1,3
1 Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA
2 Division of Cardiovascular Research, Global-Edge Institute, Tokyo Institute of Technology, Frontier S2-16, Nagatsuda, Midori-ku, Yokohama, Kanagawa 226-8503, Japan
3 Department of Pediatrics, Cardiovascular Research Institute, and Institute for Regeneration Medicine, University of California, San Francisco, California 94158, USA
Heart disease is the leading cause of mortality and morbidity in the western world. The heart has little regenerative capacity after damage, leading to much interest in understanding the factors required to produce new cardiac myocytes. Despite a robust understanding of the molecular networks regulating cardiac differentiation1, 2, no single transcription factor or combination of factors has been shown to activate the cardiac gene program de novo in mammalian cells or tissues. Here we define the minimal requirements for transdifferentiation of mouse mesoderm to cardiac myocytes. We show that two cardiac transcription factors, Gata4 and Tbx5, and a cardiac-specific subunit of BAF chromatin-remodelling complexes, Baf60c (also called Smarcd3), can direct ectopic differentiation of mouse mesoderm into beating cardiomyocytes, including the normally non-cardiogenic posterior mesoderm and the extraembryonic mesoderm of the amnion. Gata4 with Baf60c initiated ectopic cardiac gene expression. Addition of Tbx5 allowed differentiation into contracting cardiomyocytes and repression of non-cardiac mesodermal genes. Baf60c was essential for the ectopic cardiogenic activity of Gata4 and Tbx5, partly by permitting binding of Gata4 to cardiac genes, indicating a novel instructive role for BAF complexes in tissue-specific regulation. The combined function of these factors establishes a robust mechanism for controlling cellular differentiation, and may allow reprogramming of new cardiomyocytes for regenerative purposes.
