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哺乳动物肌管的脱差是由msx1诱导的

S J Odelberg¹, A Kollhoff, M T Keating

¹Division of Cardiology, Department of Internal Medicine, University of Utah, Salt Lake City, UT 84112, USA. odelberg@howard.genetics.utah.edu

|February 13, 2001

概括

以前认为不可逆转的终端分化哺乳动物细胞可以脱差. 异卵性msx1表达在小鼠肌管中诱导了脱差异化,使其能够重新分化为多种细胞类型.

科学领域:

细胞生物学细胞生物学
发育生物学发展生物学
肌肉干细胞研究肌肉干细胞研究

背景情况:

细胞分化通常被认为是哺乳动物的终端和不可逆转的过程.
终端分化的细胞保持了专门的功能,但失去了增殖潜力.

研究的目的:

为了研究终端分化哺乳动物髓管脱差的潜力.
探索 msx1 在启动肌管脱差的作用.

主要方法:

使用C2C12小鼠肌管作为模型系统.
诱导了msx1基因的子宫外表达.
评估肌肉特异性蛋白质 (MyoD,myogenin,MRF4,p21) 的变化.
分析了细胞形态,增殖和克隆群.

主要成果:

宫外MSX1表达减少了关键肌肉蛋白质在20%-50%的肌管.
大约9%的髓管经历了裂变,形成较小的髓管或增殖单核细胞.
衍生的单核细胞可以重新分化为chondrogenic,adipogenic,myogenic和osteogenic血统.

结论:

终端分化的哺乳动物肌管可以在适当的刺激下脱差.
Msx1在促进这种髓管分离过程中发挥着作用.
不分化的细胞保留多能性,这表明终端分化的细胞具有可塑性.

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