Bile acid and inflammation activate gastric cardia stem cells in a mouse model of barrett-like metaplasia

QuanteM.; BhagatG.; AbramsJ.A.; MaracheF.; GoodP.; LeeM.D.; LeeY.; FriedmanR.; AsfahaS.; DubeykovskayaZ.; MahmoodU.; FigueiredoJ.-L.; KitajewskiJ.; ShawberC.; LightdaleC.J.; RustgiA.K.; WangT.C.

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Bile acid and inflammation activate gastric cardia stem cells in a mouse model of barrett-like metaplasia

机译：胆汁酸和炎症激活Barrett样化生小鼠模型中的胃card门干细胞

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Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and EAC. Histopathology and gene signatures closely resembled human BE, with upregulation of TFF2, Bmp4, Cdx2, Notch1, and IL-6. The development of BE and EAC was accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency. Lgr5 + gastric cardia stem cells present in BE were able to lineage trace the early BE lesion. Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promoting IL-1β-IL-6 signaling cascade and Dll1-dependent Notch signaling.

机译：食道腺癌（EAC）源于Barrett食道（BE），这是与反流性食管炎相关的肠样柱状化生。在BE的转基因小鼠模型中，食管白细胞介素-1β表型的食管过度表达会复制人类病理学，并伴有食管炎，Barrett样化生和EAC的演变。组织病理学和基因特征与人类BE非常相似，TFF2，Bmp4，Cdx2，Notch1和IL-6上调。暴露于胆汁酸和/或亚硝胺可加速BE和EAC的发展，并受到IL-6缺乏的抑制。 BE中存在的Lgr5 +胃card门干细胞能够沿谱追溯早期BE病变。我们的数据表明BE和EAC来自胃祖细胞，这是由于肿瘤促进性IL-1β-IL-6信号级联和Dll1依赖性Notch信号传导。

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《Cancer Cell》 |2012年第1期|共16页
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QuanteM.; BhagatG.; AbramsJ.A.; MaracheF.; GoodP.; LeeM.D.; LeeY.; FriedmanR.; AsfahaS.; DubeykovskayaZ.; MahmoodU.; FigueiredoJ.-L.; KitajewskiJ.; ShawberC.; LightdaleC.J.; RustgiA.K.; WangT.C.;
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1. Bile acid and inflammation activate gastric cardia stem cells in a mouse model of barrett-like metaplasia [J] . QuanteM., BhagatG., AbramsJ.A., Cancer Cell . 2012,第1期

机译：胆汁酸和炎症激活Barrett样化生小鼠模型中的胃card门干细胞
2. Involvement of membrane-type bile acid receptor M-BAR/TGR5 in bile acid-induced activation of epidermal growth factor receptor and mitogen-activated protein kinases in gastric carcinoma cells. [J] . Yasuda H, Hirata S, Inoue K, Biochemical and Biophysical Research Communications . 2007,第1期

机译：膜型胆汁酸受体M-BAR / TGR5参与胆汁酸诱导的胃癌细胞中表皮生长因子受体和丝裂原活化蛋白激酶的活化。
3. Distinct intestinal adaptation for vitamin B12 and bile acid absorption revealed in a new mouse model of massive ileocecal resection Distinct intestinal adaptation for vitamin B12 and bile acid absorption revealed in a new mouse model of massive ileocecal resection Distinct intestinal adaptation for vitamin B12 and bile acid absorption revealed in a new mouse model of massive ileocecal resection [J] . Shintaro Akiyama, Wakana Mochizuki, Kengo Nozaki, Biology Open . 2017,第9期

机译：在新的大规模回盲肠切除术小鼠模型中显示出肠道对维生素B12和胆汁酸吸收的独特适应性在新的大规模回盲肠切除术小鼠模型中显示出对肠道维生素B12和胆汁酸的独特吸收适应性在大型回盲肠切除术的新小鼠模型中发现
4. Metabolic Phenotyping of Bile Acids - Standardized quantitative bile acids analysis in human plasma/serum and mouse plasma on different (U)HPLC-MS/MS platforms. [C] . Hai Pham Tuan, Doreen Kirchberg, Ines Zitturi, International Mass Spectrometry Conference . 2014

机译：胆汁酸的代谢表型 - 在不同（U）HPLC-MS / MS平台上的人血浆/血清和小鼠血浆中标准化的定量胆汁酸分析。
5. Cell specific regulation of sonic hedgehog in adult stomach: Understanding mechanisms leading to gastric atrophy/metaplasia. [D] . Waghray, Meghna. 2009

机译：成年胃中声波刺猬的细胞特异性调节：了解导致胃萎缩/转移的机制。
6. Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett’s-like metaplasia [O] . Michael Quante, Govind Bhagat, Julian Abrams, -1

机译：胆汁酸和炎症激活贲门茎中的Barretts样化生小鼠模型细胞
7. Bile Acid and Inflammation Activate Gastric Cardia Stem Cells in a Mouse Model of Barrett-Like Metaplasia [O] . Quante Michael, Bhagat Govind, Abrams Julian A., 2012

机译：胆汁酸和炎症激活Barrett样化生小鼠模型中的胃Card门干细胞。
8. Bile Acids are not Equally Damaging to the Gastric Mucosa. [R] . Harmon, J. W., Doong, T., Gadacz, T. R. 1978

机译：胆汁酸不会对胃粘膜造成同样的损害。

Bile acid and inflammation activate gastric cardia stem cells in a mouse model of barrett-like metaplasia

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