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. 2019 May 24;20(10):2549.
doi: 10.3390/ijms20102549.

RETRACTED: Regulation of Long Non-Coding RNA-Dreh Involved in Proliferation and Migration of Hepatic Progenitor Cells during Liver Regeneration in Rats

Affiliations

RETRACTED: Regulation of Long Non-Coding RNA-Dreh Involved in Proliferation and Migration of Hepatic Progenitor Cells during Liver Regeneration in Rats

Zhiyan Ruan et al. Int J Mol Sci. .

Retraction in

Abstract

Liver regeneration plays a significant role in protecting liver function after liver injury or chronic liver disease. Long non-coding RNAs (lncRNAs) are considered to be involved in the proliferation of hepatocytes and liver regeneration. Therefore, this study aimed to explore the effects of LncRNA-Dreh on the regulation of hepatic progenitor cells (HPCs) during liver regeneration in rats. Initially, the rat model of liver injury was established to investigate the effect of LncRNA-Dreh down-regulation on liver tissues of rats with liver injury. Subsequently, HPCs line WB-F344 cells were transfected with interference plasmid of LncRNA-Dreh and the expression of LncRNA-Dreh and Vimentin was detected. The proliferation and migration ability of WB-F344 cells, as well as the content of albumin (ALB) and alpha fetoprotein (AFP) in cell differentiation were then determined. Disorderly arranged structure of liver tissue, a large number of HPCs set portal area as center extended to hepatic lobule and ductular reaction were observed in liver tissues of rats with liver injury. The expression of LncRNA-Dreh decreased while Vimentin increased in liver tissues of rats with liver injury. Moreover, the proliferation and migration ability, expression of Vimentin and AFP in WB-F344 cells were increased after silencing of LncRNA-Dreh and ALB was decreased. Collectively, our findings demonstrate that inhibition of LncRNA-Dreh can enhance the proliferation and migration abilities of HPCs in liver regeneration but cause abnormal differentiation of HPCs.

Keywords: albumin; alpha fetoprotein; hepatic progenitor cell; liver injury; liver regeneration; long non-coding RNA-Dreh; vimentin.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Liver tissues are disorderly arranged in rats with liver injury and appeared ductular reaction. HE, hematoxylin-eosin; NC, negative control by polyethylene glycol (PEG) solution. Ten rats in each group. Scale bars represent 25 μm.
Figure 2
Figure 2
Liver tissues of rats with liver injury exhibit decreased LncRNA-Dreh. * p < 0.05, vs. the normal by water and NC groups by PEG solution. The results are given as means ± SD (n = 10 rats). Statistical analyses were performed according to ANOVA with chi-square test (p < 0.05).
Figure 3
Figure 3
Liver tissues of rats with liver injury exhibited increased Vimentin expression. Panel (A), mRNA expression of Vimentin in liver tissue of rats with liver injury measured by RT-qPCR; panel (B,C), the protein expression of Vimentin in liver tissue of rats with liver injury measured by Western blot; * p < 0.05, vs. the normal by water and NC groups by PEG solution. The results are given as means ± SD (n = 10 rats). Enumeration data were performed according to ANOVA with chi-square test (p < 0.05).
Figure 4
Figure 4
The WB-F344 cells proliferation is elevated after silencing of LncRNA-Dreh. * p < 0.05, vs. the blank and control groups. Cells without any transfection were used as the blank group, cells with blank plasmid transfection were used as the control group. The results are given as means ± SD (n = 3 samples). Enumeration data were performed according to ANOVA with chi-square test (p < 0.05).
Figure 5
Figure 5
The WB-F344 cells migration is enhanced after silencing of LncRNA-Dreh. * p < 0.05, vs. the blank and control groups. (A) the Transwell assay of WB-F344 cells proliferation; Scale bars represent 50 μm. (B) the number of migrated cells of the blank, control and si-Dreh groups. Cells without any transfection were used as the blank group, cells with blank plasmid transfection were used as the control group. The results are given as means ± SD (n = 3 samples). Enumeration data were performed according to ANOVA with chi-square test (p < 0.05).
Figure 6
Figure 6
The Vimentin expression of WB-F344 cells increases after silencing of LncRNA-Dreh. (A) mRNA expression of Vimentin increased in WB-F344 cells after inhibition of LncRNA-Dreh measured by RT-qPCR; (B) the density of Vimentin and β-actin in WB-F344 cells of the blank, control and si-Dreh groups; (C) relative expression of Vimentin increased in WB-F344 cells after inhibition of LncRNA-Dreh measured by Western blot analysis; * p < 0.05, vs. the blank and control groups. Cells without any transfection were used as the blank group, cells with blank plasmid transfection were used as the control group. The results are given as means ± SD (n = 3 samples). Enumeration data were performed according to ANOVA with chi-square test (p < 0.05).
Figure 7
Figure 7
The synthesis ability of ALB and AFP during the differentiation of WB-F344 is changed after LncRNA-Dreh silencing. (A) synthesis ability of ALB is decreased during the differentiation of WB-F344 after LncRNA-Dreh silencing; (B) synthesis ability of AFP is increased during the differentiation of WB-F344 after LncRNA-Dreh silencing. * p < 0.05, vs. the blank and control groups at the 6th, 9th, 12th, 15th and 18th day. Cells without any transfection were used as the blank group, cells with blank plasmid transfection were used as the control group. The results are given as means ± SD (n = 3 samples). Enumeration data were performed according to ANOVA with chi-square test (p < 0.05).

References

    1. Michalopoulos G.K. Hepatostat: Liver regeneration and normal liver tissue maintenance. Hepatology. 2017;65:1384–1392. doi: 10.1002/hep.28988. - DOI - PubMed
    1. Mao S.A., Glorioso J.M., Nyberg S.L. Liver regeneration. Transl. Res. 2014;163:352–362. doi: 10.1016/j.trsl.2014.01.005. - DOI - PMC - PubMed
    1. Kogure T., Yan I.K., Lin W.L., Patel T. Extracellular Vesicle-Mediated Transfer of a Novel Long Noncoding RNA TUC339: A Mechanism of Intercellular Signaling in Human Hepatocellular Cancer. Genes Cancer. 2013;4:261–272. doi: 10.1177/1947601913499020. - DOI - PMC - PubMed
    1. Van Haele M., Roskams T. Hepatic Progenitor Cells: An Update. Gastroenterol. Clin. North Am. 2017;46:409–420. doi: 10.1016/j.gtc.2017.01.011. - DOI - PubMed
    1. Li J., Jin W., Qin Y., Zhao W., Chang C., Xu C. Expression Profile and Function Analysis of LncRNAs during Priming Phase of Rat Liver Regeneration. PLoS ONE. 2016;11:e0156128. doi: 10.1371/journal.pone.0156128. - DOI - PMC - PubMed

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