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874 results on '"Ren, Fazheng"'

6. Lepr+ mesenchymal cells sense diet to modulate intestinal stem/progenitor cells via Leptin–Igf1 axis

Author

Deng, Min, Guerrero-Juarez, Christian F, Sheng, Xiaole, Xu, Jiuzhi, Wu, Xi, Yao, Kai, Li, Mengzhen, Yang, Xu, Li, Guilin, Xiao, Jintao, Liu, Xiaowei, Wu, Kaichun, Ren, Fazheng, Nie, Qing, Plikus, Maksim V, Yu, Zhengquan, and Lv, Cong

Subjects
Biochemistry and Cell Biology, Biological Sciences, Stem Cell Research - Nonembryonic - Non-Human, Digestive Diseases, Nutrition, Stem Cell Research - Nonembryonic - Human, Regenerative Medicine, Stem Cell Research, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Oral and gastrointestinal, Diet, Intestinal Mucosa, Leptin, Mesenchymal Stem Cells, Stem Cells, Lepr+ mesenchymal cells, niche, intestinal stem cells, high fat diet, fasting, Clinical Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

Diet can impact on gut health and disease by modulating intestinal stem cells (ISCs). However, it is largely unknown if and how the ISC niche responds to diet and influences ISC function. Here, we demonstrate that Lepr+ mesenchymal cells (MCs) surrounding intestinal crypts sense diet change and provide a novel niche signal to maintain ISC and progenitor cell proliferation. The abundance of these MCs increases upon administration of a high-fat diet (HFD) but dramatically decreases upon fasting. Depletion of Lepr+ MCs resulted in fewer intestinal stem/progenitor cells, compromised the architecture of crypt-villus axis and impaired intestinal regeneration. Furthermore, we showed that IGF1 secreted by Lepr+ MCs is an important effector that promotes proliferation of ISCs and progenitor cells in the intestinal crypt. We conclude that Lepr+ MCs sense diet alterations and, in turn, modulate intestinal stem/progenitor cell function via a stromal IGF1-epithelial IGF1R axis. These findings reveal that Lepr+ MCs are important mediators linking systemic diet changes to local ISC function and might serve as a novel therapeutic target for gut diseases.

Published
2022

12. Metagenome-wide analysis uncovers gut microbial signatures and implicates taxon-specific functions in end-stage renal disease

Author

Zhang, Pan, Wang, Xifan, Li, Shenghui, Cao, Xuesen, Zou, Jianzhou, Fang, Yi, Shi, Yiqin, Xiang, Fangfang, Shen, Bo, Li, Yixuan, Fang, Bing, Zhang, Yue, Guo, Ruochun, Lv, Qingbo, Zhang, Liwen, Lu, Yufei, Wang, Yaqiong, Yu, Jinbo, Xie, Yeqing, Wang, Ran, Chen, Xiaohong, Yu, Jiawei, Zhang, Zhen, He, Jingjing, Zhan, Jing, Lv, Wenlv, Nie, Yuxin, Cai, Jieru, Xu, Xialian, Hu, Jiachang, Zhang, Qi, Gao, Ting, Jiang, Xiaotian, Tan, Xiao, Xue, Ning, Wang, Yimei, Ren, Yimei, Wang, Li, Zhang, Han, Ning, Yichun, Chen, Jing, Zhang, Lin, Jin, Shi, Ren, Fazheng, Ehrlich, Stanislav Dusko, Zhao, Liang, and Ding, Xiaoqiang

Published
2023
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28. Author Correction: MiR-31 promotes mammary stem cell expansion and breast tumorigenesis by suppressing Wnt signaling antagonists.

Author

Lv, Cong, Li, Fengyin, Li, Xiang, Tian, Yuhua, Zhang, Yue, Sheng, Xiaole, Song, Yongli, Meng, Qingyong, Yuan, Shukai, Luan, Liming, Andl, Thomas, Feng, Xu, Jiao, Baowei, Xu, Mingang, Plikus, Maksim V, Dai, Xing, Lengner, Christopher, Cui, Wei, Ren, Fazheng, Shuai, Jianwei, Millar, Sarah E, and Yu, Zhengquan

Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2020

29. The Msi1-mTOR pathway drives the pathogenesis of mammary and extramammary Paget’s disease

Author

Song, Yongli, Guerrero-Juarez, Christian F, Chen, Zhongjian, Tang, Yichen, Ma, Xianghui, Lv, Cong, Bi, Xueyun, Deng, Min, Bu, Lina, Tian, Yuhua, Liu, Ruiqi, Zhao, Ran, Xu, Jiuzhi, Sheng, Xiaole, Du, Sujuan, Liu, Yeqiang, Zhu, Yunlu, Shan, Shi-jun, Chen, Hong-duo, Zhao, Yiqiang, Zhou, Guangbiao, Shuai, Jianwei, Ren, Fazheng, Xue, Lixiang, Ying, Zhaoxia, Dai, Xing, Lengner, Christopher J, Andersen, Bogi, Plikus, Maksim V, Nie, Qing, and Yu, Zhengquan

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Cancer, 2.1 Biological and endogenous factors, Adult, Aged, Animals, Antibiotics, Antineoplastic, Biomarkers, Breast Neoplasms, Female, Humans, Male, Mice, Middle Aged, Nerve Tissue Proteins, Paget Disease, Extramammary, RNA-Binding Proteins, Sirolimus, TOR Serine-Threonine Kinases, Clinical Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

Mammary and extramammary Paget's Diseases (PD) are a malignant skin cancer characterized by the appearance of Paget cells. Although easily diagnosed, its pathogenesis remains unknown. Here, single-cell RNA-sequencing identified distinct cellular states, novel biomarkers, and signaling pathways - including mTOR, associated with extramammary PD. Interestingly, we identified MSI1 ectopic overexpression in basal epithelial cells of human PD skin, and show that Msi1 overexpression in the epidermal basal layer of mice phenocopies human PD at histopathological, single-cell and molecular levels. Using this mouse model, we identified novel biomarkers of Paget-like cells that translated to human Paget cells. Furthermore, single-cell trajectory, RNA velocity and lineage-tracing analyses revealed a putative keratinocyte-to-Paget-like cell conversion, supporting the in situ transformation theory of disease pathogenesis. Mechanistically, the Msi1-mTOR pathway drives keratinocyte-Paget-like cell conversion, and suppression of mTOR signaling with Rapamycin significantly rescued the Paget-like phenotype in Msi1-overexpressing transgenic mice. Topical Rapamycin treatment improved extramammary PD-associated symptoms in humans, suggesting mTOR inhibition as a novel therapeutic treatment in PD.

Published
2020

30. Cycling Stem Cells Are Radioresistant and Regenerate the Intestine

Author

Sheng, Xiaole, Lin, Ziguang, Lv, Cong, Shao, Chunlei, Bi, Xueyun, Deng, Min, Xu, Jiuzhi, Guerrero-Juarez, Christian F, Li, Mengzhen, Wu, Xi, Zhao, Ran, Yang, Xu, Li, Guilin, Liu, Xiaowei, Wang, Qingyu, Nie, Qing, Cui, Wei, Gao, Shan, Zhang, Hongquan, Liu, Zhihua, Cong, Yingzi, Plikus, Maksim V, Lengner, Christopher J, Andersen, Bogi, Ren, Fazheng, and Yu, Zhengquan

Subjects
Biological Sciences, Genetics, Digestive Diseases, Stem Cell Research - Nonembryonic - Non-Human, Stem Cell Research, Regenerative Medicine, Stem Cell Research - Nonembryonic - Human, 2.1 Biological and endogenous factors, Animals, Cell Lineage, Female, Homeostasis, Intestinal Mucosa, Intestines, Male, Mice, Nerve Tissue Proteins, Paneth Cells, RNA-Binding Proteins, Radiation Tolerance, Receptors, G-Protein-Coupled, Regeneration, Sequence Analysis, RNA, Single-Cell Analysis, Stem Cells, DNA damage response, Msi1, epithelial regeneration, intestinal stem cells, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

A certain number of epithelial cells in intestinal crypts are DNA damage resistant and contribute to regeneration. However, the cellular mechanism underlying intestinal regeneration remains unclear. Using lineage tracing, we show that cells marked by an Msi1 reporter (Msi1+) are right above Lgr5high cells in intestinal crypts and exhibit DNA damage resistance. Single-cell RNA sequencing reveals that the Msi1+ cells are heterogeneous with the majority being intestinal stem cells (ISCs). The DNA damage-resistant subpopulation of Msi1+ cells is characterized by low-to-negative Lgr5 expression and is more rapidly cycling than Lgr5high radiosensitive crypt base columnar stem cells (CBCs). This enables an efficient repopulation of the intestinal epithelium at early stage when Lgr5high cells are not emerging. Furthermore, relative to CBCs, Msi1+ cells preferentially produce Paneth cells during homeostasis and upon radiation repair. Together, we demonstrate that the DNA damage-resistant Msi1+ cells are cycling ISCs that maintain and regenerate the intestinal epithelium.

Published
2020

45. Enhancement of Mechanical Properties of Zein-Based Nanofibers by Incorporation of Millet Gliadin.

Author

Wang, Shumin, Wang, Pengjie, Liu, Siyuan, Wang, Ran, Li, Yixuan, Wang, Xiaoyu, Ren, Fazheng, Luo, Jie, and Fang, Bing

Subjects
HYDROGEN bonding interactions, TRANSMISSION electron microscopy, MOLECULAR structure, INFRARED spectra, ACETIC acid
Abstract

In this work, a novel reinforcing filler, millet gliadin (MG), was used for the improvement of the mechanical properties of zein nanofibers. The structural and physicochemical properties of MG were compared with those of zein, and the influence of MG on the morphology, physical properties, and molecular structure of zein nanofibers was investigated. The results indicated that MG has an obviously smaller weight-average molecular weight (7623) in comparison to zein (13,330). Transmission electron microscopy showed that zein molecules more easily form aggregates with larger diameters than MG molecules in acetic acid. At a concentration of 30% (w/v), MG exhibited a significantly higher viscosity (0.66 ± 0.03 Pa·s) than zein (0.32 ± 0.01 Pa·s), indicating the stronger interactions of MG molecules. With the incorporation of MG, the tensile strength was significantly increased to 49.32 MPa (ZM-1/2), which is 2.08 times and 4.45 times higher than that of pure zein nanofibers (ZM-1/0) and MG nanofibers (ZM-0/1-1), respectively. Moreover, zein/MG composite nanofibers exhibited improved water stability. Fourier transform infrared spectra showed evidence of the hydrogen bonding interaction between zein and MG. Therefore, MG is a good candidate for use as a natural reinforcing filler in electrospun nanofibers made of biopolymers. [ABSTRACT FROM AUTHOR]

Published
2024
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49. MiR-31 promotes mammary stem cell expansion and breast tumorigenesis by suppressing Wnt signaling antagonists.

Author

Lv, Cong, Li, Fengyin, Li, Xiang, Tian, Yuhua, Zhang, Yue, Sheng, Xiaole, Song, Yongli, Meng, Qingyong, Yuan, Shukai, Luan, Liming, Andl, Thomas, Feng, Xu, Jiao, Baowei, Xu, Mingang, Plikus, Maksim V, Dai, Xing, Lengner, Christopher, Cui, Wei, Ren, Fazheng, Shuai, Jianwei, Millar, Sarah E, and Yu, Zhengquan

Subjects
Mammary Glands, Human, Cell Line, Tumor, Stem Cells, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Mice, Breast Neoplasms, NF-kappa B, MicroRNAs, Cell Proliferation, Down-Regulation, Gene Expression Regulation, Neoplastic, Female, Wnt Proteins, beta Catenin, Neoplastic Stem Cells, Wnt Signaling Pathway, Cell Self Renewal, Stem Cell Research - Nonembryonic - Human, Breast Cancer, Stem Cell Research, Stem Cell Research - Nonembryonic - Non-Human, Cancer, Biotechnology, Genetics, 2.1 Biological and endogenous factors, Mammary Glands, Human, Cell Line, Tumor, Inbred C57BL, Transgenic, Gene Expression Regulation, Neoplastic
Abstract

MicroRNA-mediated post-transcriptional regulation plays key roles in stem cell self-renewal and tumorigenesis. However, the in vivo functions of specific microRNAs in controlling mammary stem cell (MaSC) activity and breast cancer formation remain poorly understood. Here we show that miR-31 is highly expressed in MaSC-enriched mammary basal cell population and in mammary tumors, and is regulated by NF-κB signaling. We demonstrate that miR-31 promotes mammary epithelial proliferation and MaSC expansion at the expense of differentiation in vivo. Loss of miR-31 compromises mammary tumor growth, reduces the number of cancer stem cells, as well as decreases tumor-initiating ability and metastasis to the lung, supporting its pro-oncogenic function. MiR-31 modulates multiple signaling pathways, including Prlr/Stat5, TGFβ and Wnt/β-catenin. Particularly, it activates Wnt/β-catenin signaling by directly targeting Wnt antagonists, including Dkk1. Importantly, Dkk1 overexpression partially rescues miR31-induced mammary defects. Together, these findings identify miR-31 as the key regulator of MaSC activity and breast tumorigenesis.

Published
2017

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