| Title |
Upregulation of hydroxysteroid sulfotransferase 2B1b promotes hepatic oval cell proliferation by modulating oxysterol-induced LXR activation in a mouse model of liver injury
|
|---|---|
| Published in |
Archives of Toxicology, April 2016
|
| DOI | 10.1007/s00204-016-1693-z |
| Pubmed ID | |
| Authors |
Zhengyang Wang, Xiaoming Yang, Liang Chen, Xiuling Zhi, Hanyu Lu, Yanxia Ning, Joe Yeong, Sifeng Chen, Lianhua Yin, Xinhong Wang, Xiaobo Li |
| Abstract |
Hydroxysteroid sulfotransferase 2B1b (SULT2B1b) sulfates cholesterol and oxysterols. Hepatic oval cells (HOCs), thought to be progenitor cells, can be triggered in chemically injured livers. The present study focused on the role of SULT2B1b in HOC proliferation after liver injury. Our experiments revealed that the expression of SULT2B1b was increased dramatically in a chemical-induced liver injury model, mainly in HOCs. Upon challenge with a hepatotoxic diet containing 0.1 % 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC), SULT2B1(-/-) mice presented alleviated liver injury and less HOC proliferation compared with wild-type (WT) mice, and these findings were verified by serum analysis, histopathology, immunofluorescence staining, RNA-seq, and Western blotting. HOCs derived from SULT2B1(-/-) mice showed lower proliferative capability than those from WT mice. SULT2B1b overexpression promoted growth of the WB-F344 hepatic oval cell line, whereas SULT2B1b knockdown inhibited growth of these cells. The IL-6/STAT3 signaling pathway also was promoted by SULT2B1b. Liquid chromatography and mass spectrometry indicated that the levels of 22-hydroxycholesterol, 25-hydroxycholesterol, and 24,25-epoxycholesterol were higher in the DDC-injured livers of SULT2B1(-/-) mice than in livers of WT mice. The above oxysterols are physiological ligands of liver X receptors (LXRs), and SULT2B1b suppressed oxysterol-induced LXR activation. Additional in vivo and in vitro experiments demonstrated that LXR activation could inhibit HOC proliferation and the IL-6/STAT3 signaling pathway, and these effects could be reversed by SULT2B1b. Our data indicate that upregulation of SULT2B1b might promote HOC proliferation and aggravate liver injury via the suppression of oxysterol-induced LXR activation in chemically induced mouse liver injury. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 12 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Germany | 1 | 8% |
| Unknown | 11 | 92% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Doctoral Student | 2 | 17% |
| Student > Ph. D. Student | 2 | 17% |
| Professor | 2 | 17% |
| Researcher | 2 | 17% |
| Student > Master | 2 | 17% |
| Other | 1 | 8% |
| Unknown | 1 | 8% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 4 | 33% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 8% |
| Biochemistry, Genetics and Molecular Biology | 1 | 8% |
| Immunology and Microbiology | 1 | 8% |
| Neuroscience | 1 | 8% |
| Other | 2 | 17% |
| Unknown | 2 | 17% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 08 April 2016.
All research outputs
#20,318,358
of 22,860,626 outputs
Outputs from Archives of Toxicology
#2,364
of 2,640 outputs
Outputs of similar age
#255,132
of 301,073 outputs
Outputs of similar age from Archives of Toxicology
#30
of 36 outputs
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