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多柔比星诱导小鼠黏膜炎期间肠道上皮和间充质基因表达的变化

Alterations in epithelial and mesenchymal intestinal gene expression during doxorubicin-induced mucositis in mice.

作者信息

de Koning Barbara A E, Lindenbergh-Kortleve Dicky J, Pieters Rob, Büller Hans A, Renes Ingrid B, Einerhand Alexandra W C

机构信息

Department of Pediatrics, Divisions of Pediatric Oncology, Erasmus MC-Sophia Children's Hospital, Rotterdam, The Netherlands.

出版信息

Dig Dis Sci. 2007 Aug;52(8):1814-25. doi: 10.1007/s10620-006-9174-5. Epub 2007 Apr 6.

DOI:10.1007/s10620-006-9174-5
PMID:17415656
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1914222/
Abstract

In the current study we aimed to gain insight into epithelial-mesenchymal cross-talk and progenitor compartment modulation during doxorubicin (DOX)-induced mucositis in mice. Intestinal segments were collected on various days after DOX treatment. DOX-induced damage at day 1-2 was characterized by increased epithelial proliferation and apoptosis and a decrease in the expression of epithelial differentiation markers. Concurrently, T-cell factor-4 (TCF4) levels increased and the epithelial differentiation enhancing factor, bone morphogenic protein-4 (BMP4), decreased. During severe damage (day 3), BMP4 levels were significantly increased, which inversely correlated with epithelial proliferation. At the same time, the expression of the epithelial differentiation markers was increasing again. At day 7, BMP4 levels were down-regulated, while the levels of the epithelial differentiation markers and TCF4 were normalized again. These data suggest that in response to DOX-induced damage, BMP4 and TCF4 are modulated in such a way that homeostasis of the progenitor compartment is partly preserved.

摘要

在本研究中，我们旨在深入了解阿霉素（DOX）诱导的小鼠粘膜炎过程中的上皮-间质相互作用以及祖细胞区室调节。在DOX治疗后的不同天数收集肠段。DOX在第1-2天引起的损伤表现为上皮细胞增殖和凋亡增加，上皮分化标志物表达减少。同时，T细胞因子4（TCF4）水平升高，而上皮分化增强因子骨形态发生蛋白4（BMP4）水平降低。在严重损伤期间（第3天），BMP4水平显著升高，这与上皮细胞增殖呈负相关。与此同时，上皮分化标志物的表达再次增加。在第7天，BMP4水平下调，而上皮分化标志物和TCF4水平再次恢复正常。这些数据表明，响应DOX诱导的损伤，BMP4和TCF4以部分维持祖细胞区室稳态的方式受到调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/cebef2c31fed/10620_2006_9174_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/19d297c04d3b/10620_2006_9174_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/e00b052acce8/10620_2006_9174_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/276d1db84e3b/10620_2006_9174_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/a268a45a7d48/10620_2006_9174_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/2b2121435a73/10620_2006_9174_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/ba4d7cca91c7/10620_2006_9174_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/cebef2c31fed/10620_2006_9174_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/19d297c04d3b/10620_2006_9174_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/e00b052acce8/10620_2006_9174_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/276d1db84e3b/10620_2006_9174_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/a268a45a7d48/10620_2006_9174_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/2b2121435a73/10620_2006_9174_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/ba4d7cca91c7/10620_2006_9174_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92a6/1914222/cebef2c31fed/10620_2006_9174_Fig7_HTML.jpg

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