p21 通过 DREAM/MMB/Rb-E2F1 调节 Wnt-Notch 平衡并维持肠道干细胞稳态。

IF 6.1 2区 生物学 Q1 CELL BIOLOGY Cell Death Discovery Pub Date : 2024-09-28 DOI:10.1038/s41420-024-02192-z
Liangxia Jiang, Jie Tian, Jun Yang, Ronggang Luo, Yongjin Zhang, Chihao Shao, Bing Guo, Xiaoming Wu, Juhua Dan, Ying Luo
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摘要

众所周知,Wnt-Notch的相互作用和平衡调控对于细胞命运决定和组织再生至关重要,然而,这种平衡是如何维持的,以及Wnt-Notch通路与细胞周期调控之间是如何联系的,目前仍不清楚。通过分析 Werner 综合征背景下 p21 功能缺失导致加速衰老表型小鼠模型的分子变化,我们观察到 Wnt3 和 β-Catenin 下调,而 Notch1 和 Hes1 上调。伴随着Wnt-Notch信号的中断,p21TKO小鼠肠道隐窝中的肠干细胞区消失,Bmi1阳性细胞增加,Olfm4/Lgr5阳性细胞消失,分泌型Paneth细胞和鹅口疮细胞减少。BrdU掺入、裂解的caspase 3和Tunel检测结果表明,肠上皮的快速更替可能导致干细胞动员异常和肠隐窝干细胞库枯竭。我们进一步发现,p21的缺失导致DREAM复合物向MMB复合物转移,是肠上皮细胞快速更替的原因。重要的是,我们发现 E2F1 是 Notch1 的转录调节因子,这将 p21-DREAM/MMB/Rb-E2F1 通路与 Wnt-Notch 通路联系起来。过表达 p21 可挽救 DREAM 通路以及 Wnt-Notch 通路的失衡。总之,我们的数据确定了p21是维持肠干细胞顺序动员、增殖和平衡的重要因素。
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p21 Regulates Wnt-Notch balance via DREAM/MMB/Rb-E2F1 and maintains intestinal stem cell homeostasis.

The crosstalk and balance regulation of Wnt-Notch have been known to be essential for cell fate decision and tissue regeneration, however, how this balance is maintained and how the Wnt-Notch pathways are connected with cell cycle regulation is still not clear. By analyzing the molecular alterations in mouse model with accelerated aging phenotypes due to loss of p21 function in a Werner syndrome background, we observed that Wnt3 and β-Catenin were down-regulated, while Notch1 and Hes1 were up-regulated. This disruption in Wnt-Notch signaling was accompanied by the loss of intestinal stem cell compartment, increase in Bmi1 positive cells, loss of Olfm4/Lgr5 positive cells, and reduced secretory Paneth cells and goblet cells in the intestinal crypts of p21TKO mice. BrdU incorporation, cleaved caspase 3, and Tunel assay results revealed the fast turnover of intestinal epithelia, which may result in abnormal stem cell mobilization and exhaustion of the stem cell reservoir in the intestinal crypts. We further identified shift of DREAM complex towards MMB complex due to the loss of p21 as the cause for faster turnover of intestinal epithelia. Importantly, we identified the E2F1 as the transcriptional regulator for Notch1, which linked the p21-DREAM/MMB/Rb-E2F1 pathway with Wnt-Notch pathway. The overexpression of p21 rescued the DREAM pathway, as well as the imbalance of Wnt-Notch pathway. In summary, our data identify p21 as an important factor in maintaining sequential mobilization, proliferation, and homeostasis of intestinal stem cells.

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来源期刊
Cell Death Discovery
Cell Death Discovery Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
8.30
自引率
1.40%
发文量
468
审稿时长
9 weeks
期刊介绍: Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary. Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.
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