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Apc1638N/+ 小鼠肠道细胞成熟动力学改变。

Altered dynamics of intestinal cell maturation in Apc1638N/+ mice.

机构信息

Department of Medicine, Montefiore Medical Center, Bronx, New York 10467, USA.

出版信息

Cancer Res. 2010 Jul 1;70(13):5348-57. doi: 10.1158/0008-5472.CAN-09-4593. Epub 2010 Jun 22.

DOI:10.1158/0008-5472.CAN-09-4593
PMID:20570902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2906237/
Abstract

Novel imaging of active transcription sites in interphase nuclei of intestinal epithelial cells in situ showed that key genes associated with Wnt and Notch signaling were dynamically regulated as the cells underwent normal maturation during their migration along the mouse crypt-villus axis (CVA). However, oscillating patterns of activation of these genes were displaced along this axis in the histologically normal intestinal mucosa of Apc(1638N/+) mice before tumor development. Gene expression profiling then showed that the normal reprogramming of cells along the CVA was dampened in the Apc(1638N/+) mice, with an overrepresentation of c-myc target genes among those loci affected in the mutant mice. Moreover, in the Apc(1638N/+) mice, there was a perturbed pattern of expression of lineage-specific markers along the CVA consistent with transcription site repression of the Math1 gene, and genes encoding enzymes of every step of the tricarboxylic acid cycle were downregulated in the crypt of Apc(1638N/+) mice compared with WT, but not in the villus. These changes may alter energy metabolism and generate a pseudohypoxic state, suggested by elevated expression of Hif1alpha and its target genes. Thus, although intestinal tumors develop in Apc(1638N/+) mice on focal loss or inactivation of the WT allele, our results show that in the Apc(1638N/+) mouse, inheritance of only a single WT Apc allele perturbs the dynamic and complex reprogramming underlying normal cell maturation, which links epithelial function and homeostasis with architectural organization of the intestine.

摘要

在原位肠道上皮细胞的有丝分裂核中,新型的转录活性位点成像显示,与 Wnt 和 Notch 信号相关的关键基因在细胞沿着小鼠隐窝绒毛轴(CVA)正常成熟过程中会被动态调节。然而,在肿瘤发生前,Apc(1638N/+) 小鼠的组织学正常的肠道黏膜中,这些基因的激活模式呈振荡式变化,沿着该轴发生了位移。随后的基因表达谱分析显示,Apc(1638N/+) 小鼠中沿着 CVA 的细胞正常重编程受到抑制,在突变小鼠中受影响的基因座中 c-myc 靶基因的代表性增加。此外,在 Apc(1638N/+) 小鼠中,沿着 CVA 的谱系特异性标志物的表达模式发生了紊乱,与 Math1 基因转录活性位点的抑制一致,并且编码三羧酸循环每一步的酶的基因在 Apc(1638N/+) 小鼠的隐窝中下调,而在绒毛中没有下调。与 WT 相比,这些变化可能会改变能量代谢并产生假性缺氧状态,这是由 Hif1alpha 及其靶基因的表达升高所提示的。因此,尽管 Apc(1638N/+) 小鼠在 WT 等位基因的局灶性缺失或失活后会发展为肠道肿瘤,但我们的结果表明,在 Apc(1638N/+) 小鼠中,仅遗传单个 WT Apc 等位基因就会干扰正常细胞成熟所必需的动态和复杂的重编程,这将上皮功能和内稳态与肠道的结构组织联系起来。

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