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LGR5 and BMI1 Increase Pig Intestinal Epithelial Cell Proliferation by Stimulating WNT/beta-Catenin Signaling

文献类型: 外文期刊

作者: Li, Xiang-Guang 1 ; Wang, Zhe 3 ; Chen, Rong-Qiang 1 ; Fu, Hou-Long 1 ; Gao, Chun-Qi 1 ; Yan, Hui-Chao 1 ; Xing, Guang 1 ;

作者机构: 1.South China Agr Univ, Coll Anim Sci, Guangdong Prov Key Lab Anim Nutr Control, Natl Engn Res Ctr Breeding Swine Ind, Guangzhou 510642, Guangdong, Peoples R China

2.Guangdong Univ Technol, Sch Chem Engn & Light Ind, Dept Pharmaceut Engn, Guangzhou 510006, Guangdong, Peoples R China

3.Tianhe Foreign Language Sch, Guangzhou 510627, Guangdong, Peoples R China

4.Henan Acad Agr Sci, Minist Agr, Key Lab Anim Immunol, Zhengzhou 450002, Henan, Peoples R China

关键词: LGR5; BMI1; WNT/beta-catenin signaling; cell proliferation; intestinal epithelial cells

期刊名称:INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES ( 影响因子:5.923; 五年影响因子:6.132 )

ISSN: 1422-0067

年卷期: 2018 年 19 卷 4 期

页码:

收录情况: SCI

摘要: Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5) and B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) are markers of fast-cycling and quiescent intestinal stem cells, respectively. To determine the functions of these proteins in large animals, we investigated their effects on the proliferation of intestinal epithelial cells from pigs. Our results indicated that LGR5 and BMI1 are highly conserved proteins and that the pig proteins have greater homology with the human proteins than do mouse proteins. Overexpression of either LGR5 or BMI1 promoted cell proliferation and WNT/beta-catenin signaling in pig intestinal epithelial cells (IPEC-J2). Moreover, the activation of WNT/beta-catenin signaling by recombinant human WNT3A protein increased cell proliferation and LGR5 and BMI1 protein levels. Conversely, inhibition of WNT/beta-catenin signaling using XAV939 reduced cell proliferation and LGR5 and BMI1 protein levels. This is the first report that LGR5 and BMI1 can increase proliferation of pig intestinal epithelial cells by activating WNT/beta-catenin signaling.

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