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4 results on '"Zhaohai Cui"'

1. Maternal antibiotic exposure enhances ILC2 activation in neonates via downregulation of IFN1 signaling

Author

Haixu Xu, Xianfu Yi, Zhaohai Cui, Hui Li, Lin Zhu, Lijuan Zhang, JiaLe Chen, Xutong Fan, Pan Zhou, Mulin Jun Li, Ying Yu, Qiang Liu, Dandan Huang, Zhi Yao, and Jie Zhou

Subjects
Science
Abstract

Abstract Microbiota have an important function in shaping and priming neonatal immunity, although the cellular and molecular mechanisms underlying these effects remain obscure. Here we report that prenatal antibiotic exposure causes significant elevation of group 2 innate lymphoid cells (ILC2s) in neonatal lungs, in both cell numbers and functionality. Downregulation of type 1 interferon signaling in ILC2s due to diminished production of microbiota-derived butyrate represents the underlying mechanism. Mice lacking butyrate receptor GPR41 (Gpr41 -/- ) or type 1 interferon receptor IFNAR1 (Ifnar1 -/- ) recapitulate the phenotype of neonatal ILC2s upon maternal antibiotic exposure. Furthermore, prenatal antibiotic exposure induces epigenetic changes in ILC2s and has a long-lasting deteriorative effect on allergic airway inflammation in adult offspring. Prenatal supplementation of butyrate ameliorates airway inflammation in adult mice born to antibiotic-exposed dams. These observations demonstrate an essential role for the microbiota in the control of type 2 innate immunity at the neonatal stage, which suggests a therapeutic window for treating asthma in early life.

Published
2023
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2. Cancer associated fibroblast–derived CCL5 promotes hepatocellular carcinoma metastasis through activating HIF1α/ZEB1 axis

Author

Haixu Xu, Jie Zhao, Jinping Li, Zhifeng Zhu, Zhaohai Cui, Ran Liu, Rong Lu, Zhi Yao, and Qiong Xu

Subjects
Cytology, QH573-671
Abstract

Abstract Cancer-associated fibroblasts (CAFs) are one of the most enriched components of Hepatocellular carcinoma (HCC) microenvironment, which are tightly related to the metastasis and invasion of HCC. We identified a mechanism by which CAF-derived chemokine CCL5 enhanced HCC metastasis by triggering the HIF1α/ZEB1 axis. We demonstrated that CAFs derived from HCC tissues promoted the migration and invasion of HCC cells and facilitated metastasis to the lung of NOD/SCID mice. Then the chemokine antibody array elucidated the higher chemokine CCL5 level secreted by CAFs than by paracancerous tissue fibroblasts (PTFs). Mechanistically, we found that CAF-derived CCL5 inhibited the ubiquitination and degradation of hypoxia-inducible factor 1 alpha (HIF1α) by binding to specific receptors, maintained HIF1α under normoxia, thereby up-regulated the downstream gene zinc finger enhancer-binding protein 1 (ZEB1) and induced epithelial-mesenchymal transition (EMT), ultimately validating its ability to promote lung metastasis of HCC. And this novel mechanism may have association with poor prognosis. Taken together, targeting CAF-derived CCL5 mediated HIF1α/ZEB1 cascade possibly propose a new therapeutic route for HCC.

Published
2022
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3. Construction and identification of influenza plasmid pool imparting high yields to candidate vaccine viruses in Vero cell at low temperature

Author

Zhaohai Cui, Xia Ou, Ze Liu, Weidong Li, Xingliang Geng, and Guoyang Liao

Subjects
0301 basic medicine, viruses, Biology, Homology (biology), Virus, Madin Darby Canine Kidney Cells, Lethal Dose 50, 03 medical and health sciences, 0302 clinical medicine, Plasmid, Dogs, vaccine, Reassortant Viruses, Chlorocebus aethiops, Animals, Humans, Gene, Vero Cells, high yield, Mice, Inbred BALB C, Influenza A Virus, H3N2 Subtype, Virion, plasmid pool, Cell Biology, Original Articles, Virology, Phenotype, Vero, Cold Temperature, 030104 developmental biology, HEK293 Cells, Influenza Vaccines, 030220 oncology & carcinogenesis, Vero cell, biology.protein, Molecular Medicine, Original Article, Female, influenza, Neuraminidase, Chickens, Plasmids
Abstract

We generated plasmid pools for the rapid preparation of candidate vaccine strains, which could grow in the Vero cells at low temperature. Firstly, we cloned in the pHW2000 plasmid each of the eight gene segments (PB2, PB1, PA, hemagglutinin [HA], neuraminidase [NA], NS, NP, M) of two master donor strains (MDS), respectively, A/Yunnan/1/2005Vca(H3N2) and B/Yunnan/2/2005Vca(By), which had Vca phenotype (cold‐adapted phenotype in Vero cells). Secondly, the similar operation was implemented with each of the HA, NA and NP segments of circulating strains with epidemic potential (parental strains). The virus rescue techniques were employed in this study, according to the homology rate of HA segments between MDS and parental strains. Then, we harvested amount of new Vca virus strains. By transmission electron microscope, it could observe new viruses' diameter and length were from 100 to 120 nm. Importantly, these reassortant viruses could get high‐yield production in Vero cells at 25℃ from the beginning to the fourth generation, which was significantly differ from their original parental viruses. Additional, these production 16 new Vca strains could maintain enough antibody binding capacity and attenuation phenotype, which consisted with their MDS. So these plasmid pools constructed by mount of different influenza A and B virus gene fragments could present desired working performance and provide convenience and realization for more Vca reassortant virus as candidate vaccine strain if needing.

Published
2020

4. Downregulation of HULC Induces Ferroptosis in Hepatocellular Carcinoma via Targeting of the miR-3200-5p/ATF4 Axis

Author

Lulu Guan, Feifei Wang, Mengjiao Wang, Songfeng Han, Zhaohai Cui, Shoumin Xi, Haixu Xu, and Shipeng Li

Subjects
Aging, Carcinoma, Hepatocellular, Article Subject, Liver Neoplasms, Down-Regulation, Cell Biology, General Medicine, Biochemistry, Activating Transcription Factor 4, Gene Expression Regulation, Neoplastic, MicroRNAs, Cell Line, Tumor, Ferroptosis, Humans, RNA, Long Noncoding, Cell Proliferation
Abstract

Hepatocellular carcinoma is a malignant tumor that poses a serious threat to human health. Ferroptosis, which represents an identified type of regulated iron-dependent cell death, may play an important role in hepatocellular carcinoma. However, it is unclear as to whether ferroptosis is involved with the mechanisms of lncRNA HULC in liver cancer cells. Here, we show that knockdown of HULC increases ferroptosis and oxidative stress in liver cancer cells. We also found changes in some related miRNAs in cells treated with HULC siRNA. Differential miRNA expression levels were determined with the use of high-throughput sequencing and prediction target genes identified using bioinformatics analysis. HULC was found to function as a ceRNA of miR-3200-5p, and miR-3200-5p regulates ferroptosis by targeting ATF4, resulting in the inhibition of proliferation and metastasis within HCC cells. In summary, these findings illuminate some of the molecular mechanisms through which downregulation of HULC induces liver cancer cell ferroptosis by targeting the miR-3200-5p/ATF4 axis to modulate the development of hepatocellular carcinoma.

Published
2021

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