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通过Ccndbp1-Atm-Chk2途径的DNA损伤反应参与葡聚糖硫酸钠诱导的小鼠结肠炎

Involvement of DNA Damage Response via the Ccndbp1-Atm-Chk2 Pathway in Mice with Dextran-Sodium-Sulfate-Induced Colitis.

作者信息

Horigome Ryoko, Kamimura Kenya, Niwa Yusuke, Ogawa Kohei, Mizuno Ken-Ichi, Fujisawa Koichi, Yamamoto Naoki, Takami Taro, Sugano Tomoyuki, Sakamaki Akira, Kamimura Hiroteru, Takamura Masaaki, Terai Shuji

机构信息

Division of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan.

Department of General Medicine, Niigata University School of Medicine, Niigata 951-8510, Japan.

出版信息

J Clin Med. 2022 Jun 25;11(13):3674. doi: 10.3390/jcm11133674.

DOI:10.3390/jcm11133674
PMID:35806959
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9267230/
Abstract

The dextran sodium sulfate (DSS)-induced colitis mouse model has been widely utilized for human colitis research. While its mechanism involves a response to double-strand deoxyribonucleic acid (DNA) damage, ataxia telangiectasia mutated (Atm)-checkpoint kinase 2 (Chk2) pathway activation related to such response remains unreported. Recently, we reported that cyclin D1-binding protein 1 () activates the pathway reflecting DNA damage in its knockout mice. Thus, this study aimed to examine the contribution of and the Atm-Chk2 pathway in DSS-induced colitis. We assessed the effect of DSS-induced colitis on colon length, disease activity index, and histological score and on the Atm-Chk2 pathway and the subsequent apoptosis in -knockout mice. DSS-induced colitis showed distal colon-dominant Atm and Chk2 phosphorylation, increase in TdT-mediated dUTP-biotin nick end labeling and cleaved caspase 3-positive cells, and histological score increase, causing disease activity index elevation and colon length shortening. These changes were significantly ameliorated in -knockout mice. In conclusion, contributed to Atm-Chk2 pathway activation in the DSS-induced colitis mouse model, causing inflammation and apoptosis of mucosal cells in the colon.

摘要

葡聚糖硫酸钠（DSS）诱导的结肠炎小鼠模型已被广泛用于人类结肠炎研究。虽然其机制涉及对双链脱氧核糖核酸（DNA）损伤的反应，但与这种反应相关的共济失调毛细血管扩张突变（Atm）-检查点激酶2（Chk2）途径的激活尚未见报道。最近，我们报道细胞周期蛋白D1结合蛋白1（）在其基因敲除小鼠中激活了反映DNA损伤的途径。因此，本研究旨在探讨在DSS诱导的结肠炎中及Atm-Chk2途径的作用。我们评估了DSS诱导的结肠炎对结肠长度、疾病活动指数、组织学评分以及对Atm-Chk2途径和基因敲除小鼠随后的细胞凋亡的影响。DSS诱导的结肠炎表现为远端结肠为主的Atm和Chk2磷酸化、末端脱氧核苷酸转移酶介导的dUTP生物素缺口末端标记增加和裂解的半胱天冬酶3阳性细胞增加，以及组织学评分增加，导致疾病活动指数升高和结肠长度缩短。这些变化在基因敲除小鼠中得到显著改善。总之，在DSS诱导的结肠炎小鼠模型中促成了Atm-Chk2途径的激活，导致结肠黏膜细胞的炎症和凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/2eede8b5b36c/jcm-11-03674-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/78fd215b3d4a/jcm-11-03674-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/dc88d0e21009/jcm-11-03674-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/5e11e49d3896/jcm-11-03674-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/a0a82e554ee8/jcm-11-03674-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/2eede8b5b36c/jcm-11-03674-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/78fd215b3d4a/jcm-11-03674-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/dc88d0e21009/jcm-11-03674-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/5e11e49d3896/jcm-11-03674-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/a0a82e554ee8/jcm-11-03674-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/9267230/2eede8b5b36c/jcm-11-03674-g005.jpg

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本文引用的文献

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2
Maintains Genome Stability in Ulcerative Colitis Regulating Anaphase-Promoting Complex Subunit 7.通过调控后期促进复合体亚基7维持溃疡性结肠炎中的基因组稳定性
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Ulcerative colitis.溃疡性结肠炎。
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Live to die another way: modes of programmed cell death and the signals emanating from dying cells.以另一种方式存活至死亡：程序性细胞死亡的模式及垂死细胞发出的信号。
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