肝脏组织再生比预想的简单
将发表在4月13日的《生物化学杂志》（The Journal of Biological Chemistry）上的文章指出，肝脏再生过程要比科学家预想的简单，这首次提供了肝细胞再生的内部机制信息，将对肝脏疾病——例如硬化、肝炎、癌症等治疗带来帮助。
哈佛医学院外科助理教授Seth Karp说：“人类肝脏是少数可以在只剩25%情况下再生的器官之一，其中机制不甚清楚，但研究结果能部分解释肝脏的这一独特性质。”
科学家已经发现参与组织再生的细胞类似胚胎期的发育器官的细胞。很多激发器官再生的蛋白已经被找到，现在科学家要激发这些蛋白来使器官再生。而肝脏再生对于需要接受肝移植的病人尤其重要。对于很多人来说，快速激发仅剩的部分肝组织再生是唯一的存活希望。
Karp小组分析了两种老鼠，一种是胚胎期的，而另一种则是移除了2/3肝脏的成年老鼠。利用DNA微阵列和其它技术，科学家希望找到帮助肝细胞生长的蛋白。
结果令人意外，科学家注意到只有很少蛋白在胚胎期和成年期肝细胞生长中都起作用。影响细胞核DNA的转录因子只在胚胎肝发育中起作用，而帮助细胞增生的蛋白则在以上两种过程中都被激发。
这表明再生肝细胞和胚胎期细胞并不一样，而且再生或许只是通过细胞增生实现。这对于医疗方面也有帮助。由于转录因子在肝再生中并不起作用，因此也许可以只激发帮助肝细胞再生的蛋白就可以了。
原始出处：http://www.physorg.com/news95530460.html
部分英文原文：
J. Biol. Chem., Vol. 282, Issue 15, 11197-11204, April 13, 2007
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Restoration of Liver Mass after Injury Requires Proliferative and Not Embryonic Transcriptional Patterns*
Hasan H. Otu
¶1, Kamila Naxerova||1, Karen Ho**2, Handan Can¶, Nicole Nesbitt**, Towia A. Libermann, and Seth J. Karp**3
From the Department of Medicine, Genomics Core, and **Department of Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, ¶Department of Genetics and Bioengineering, Yeditepe University, 34755 Istanbul, Turkey, and ||Children's Hospital Informatics Program, Boston, Massachusetts 02115
Normal adult liver is uniquely capable of renewal and repair after injury. Whether this response represents simple hyperplasia of various liver elements or requires recapitulation of the genetic program of the developing liver is not known. To study these possibilities, we examined transcriptional programs of adult liver after partial hepatectomy and contrasted these with developing embryonic liver. Principal component analysis demonstrated that the time series of gene expression during liver regeneration does not segregate according to developmental transcription patterns. Gene ontology analysis revealed that liver restoration after hepatectomy and liver development differ dramatically with regard to transcription factors and chromatin structure modification. In contrast, the tissues are similar with regard to proliferation-associated genes. Consistent with these findings, real-time polymerase chain reaction showed transcription factors known to be important in liver development are not induced during liver regeneration. These three lines of evidence suggest that at a transcriptional level restoration of liver mass after injury is best described as hepatocyte hyperplasia and not true regeneration. We speculate this novel pattern of gene expression may underlie the unique capacity of the liver to repair itself after injury.
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