Evidence map›Paper›PMID 39044218›Full record

ArticleParasites & vectors2024

The impact of ICOSL/ICOS pathway-regulated long non-coding RNAs on liver fibrosis in mice infected with Schistosoma japonicum.

Ping Huang, Jing Xu, Suqin Jiang, Yanan Zhang, Xinyi Wang, Chunrong Xiong, Chaoming Xia

Abstract read
In one paragraph

Article in Parasites & vectors, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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0cells of the map it votes in
1citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

7 authors.

Ping Huang *Department of Parasitology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, Jiangsu Province, China.
Jing Xu *Department of Parasitology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, Jiangsu Province, China.
Suqin JiangDepartment of Parasitology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, Jiangsu Province, China.
Yanan ZhangDepartment of Parasitology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, Jiangsu Province, China.
Xinyi WangDepartment of Parasitology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, Jiangsu Province, China.
Chunrong XiongJiangsu Institute of Parasitic Diseases, Wuxi City, Jiangsu Province, China.
Chaoming XiaDepartment of Parasitology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, Jiangsu Province, China. xiachaoming@suda.edu.cn.

Funding

China Postdoctoral Science Foundation 2022M712307Hainan Provincial Natural Science Foundation of China 821RC1068Jiangsu Funding Program for Excellent Postdoctoral Talent 2022ZB573National Natural Science Foundation of China 82172294Priority Academic Program Development of Jiangsu Higher Education Institutions YX13400214The Natural Science Foundation of the Jiangsu Higher Education Institutions of China 23KJD310003
6 · The paper itself

Abstract

backgroundThe primary pathogenic mechanism of schistosomiasis-associated liver fibrosis involves the deposition of schistosome eggs, leading to the formation of liver egg granulomas and subsequent liver fibrosis. Hepatic stellate cells are abnormally activated, resulting in excessive collagen deposition and fibrosis development. While specific long non-coding RNAs (lncRNAs) have been associated with fibrotic processes, their roles in schistosomiasis-associated liver fibrosis remain unclear.

methodsOur previous research indicated that downregulating the ICOSL/ICOS could partially alleviate liver fibrosis. In this study, we established a schistosomiasis infection model in C57BL/6 and ICOSL knockout (KO) mice, and the liver pathology changes were observed at various weeks postinfection (wpi) using hematoxylin and eosin and Masson's trichrome staining. Within the first 4 wpi, no significant liver abnormalities were observed. However, mice exhibited evident egg granulomas and fibrosis in their livers at 7 wpi. Notably, ICOSL-KO mice had significantly smaller pathological variations compared with simultaneously infected C57BL/6 mice. To investigate the impact of lncRNAs on schistosomiasis-associated liver fibrosis, quantitative real-time polymerase chain reaction (RT-qPCR) was used to monitor the dynamic changes of lncRNAs in hepatic stellate cells of infected mice.

resultsThe results demonstrated that lncRNA-H19, -MALAT1, -PVT1, -P21 and -GAS5 all participated in liver fibrosis formation after schistosome infection. In addition, ICOSL-KO mice exhibited significantly inhibited expression of lncRNA-H19, -MALAT1 and -PVT1 after 7 wpi. In contrast, they showed enhanced expression of lncRNA-P21 and -GAS5 compared with C57BL/6 mice, influencing liver fibrosis development. Furthermore, small interfering RNA transfection (siRNA) in JS-1 cells in vitro confirmed that lncRNA-H19, -MALAT1, and -PVT1 promoted liver fibrosis, whereas lncRNA-P21 and -GAS5 had the opposite effect on key fibrotic molecules, including α- smooth muscle actin and collagen I expression.

conclusionsThis study uncovers that ICOSL/ICOS may play a role in activating hepatic stellate cells and promoting liver fibrosis in mice infected with Schistosoma japonicum by dynamically regulating the expression of specific lncRNAs. These findings offer potential therapeutic targets for schistosomiasis-associated liver fibrosis.

Indexed as

Inducible T-Cell Co-Stimulator LigandLiver CirrhosisMice, Inbred C57BLMice, KnockoutRNA, Long NoncodingSchistosoma japonicumSchistosomiasis japonicaAnimalsDisease Models, AnimalFemaleHepatic Stellate CellsInducible T-Cell Co-Stimulator ProteinLiverMiceIcosl protein, mouseIcos protein, mouseInducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinRNA, Long NoncodingHepatic stellate cellsICOSL/ICOSLiver fibrosislncRNAsSchistosomiasis

Identifiers

PMID39044218
PMCPMC11267842

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.