Effect of knockdown splicing factor Prp17 on liver morphology and liver function in mice

MA Wen-jie, HUANG Zi-jin, DOU Jian-ping, MA Chun-mei, LIU Ai-jun, WANG Jia-you

Chinese Journal of Clinical Anatomy ›› 2020, Vol. 38 ›› Issue (2) : 194-197.

Chinese Journal of Clinical Anatomy ›› 2020, Vol. 38 ›› Issue (2) : 194-197. DOI: 10.13418/j.issn.1001-165x.2020.02.018

Effect of knockdown splicing factor Prp17 on liver morphology and liver function in mice

  • MA Wen-jie1,HUANG Zi-jin2, DOU Jian-ping1, MA Chun-mei1, LIU Ai-jun1,WANG Jia-you1
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Abstract

Objective   To investigate the effects of knockdown splicing factor Prp17 on liver morphology and liver function in mice.    Methods   The knockdown splicing factor Prp17 adenovirus (Ad-shPrp17) was constructed. C57BL/6 mice were randomly divided into a control group and an Ad-shPrp17 group with 8 mice in each group. The Ad-shPrp17 group was injected with Ad-shPrp17 through medial canthus vein. After 10 days, mouse serum and liver tissue were collected. Pathological changes of liver were observed by hematoxylin-eosin staining. The activities of serum aspartate transaminase (AST) and alanine transaminase (ALT) were determined by enzyme method. Gene expression was analyzed by fluorescence quantitative polymerase chain reaction.   Results   Compared with the control group, the Ad-shPrp17 group had the following changes: (1) Liver index and the quality of liver  significantly increased (P<0.01); (2) with scattered and swollen hepatocytes, loose cytoplasm, the liver cells changed from polygonal to round. The cytoplasm was transparent and ballooning changed, and some cells were necrotic; (3) The enzyme activities of serum ALT and AST were significantly increased (P<0.01); (4) The expression of liver tissue TNF-α and IL1-β increased (P<0.05).    Conclusions    Knockdown of splicing factor Prp17 could cause pathological changes and function damage in the liver tissue of mice, and its mechanism may be related to the induction of hepatic inflammatory response. This study provides a new therapeutic target and theoretical basis for the prevention and treatment of liver diseases.

Key words

Splicing factor;  Prp17 /  Liver morphology /  Liver function /  Inflammation

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MA Wen-jie, HUANG Zi-jin, DOU Jian-ping, MA Chun-mei, LIU Ai-jun, WANG Jia-you. Effect of knockdown splicing factor Prp17 on liver morphology and liver function in mice[J]. Chinese Journal of Clinical Anatomy. 2020, 38(2): 194-197 https://doi.org/10.13418/j.issn.1001-165x.2020.02.018

References

[1] Pan Q, Shai O, Lee LJ,et al. Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing[J]. Nat Genet, 2008, 40(12): 1413-1415.
[2] Wang J, Kainrad N, Shen T, et al. Hepatic knockdown of splicing regulator slu7 ameliorates inflammation and attenuates liver injury in ethanol-fed mice[J]. Am J Pathol, 2018, 188(8): 1807-1819.
[3]  Kaplan Y, Kupiec M. A role for the yeast cell cycle/splicing factor Cdc40 in the G1/S transition[J]. Curr Genet, 2007, 51(2): 123-140.
[4]  Kong XX, Lv YR, Shao LP, et al. HBx-induced MiR-1269b in NF-κB dependent manner upregulates cell division cycle 40 homolog (CDC40) to promote proliferation and migration in hepatoma cells[J]. J Transl Med, 2016, 14(1): 189-202.
[5]  Cheng Y, Luo C, Wu W, et al. Liver-Specific Deletion of SRSF2 caused acute liver failure and early death in mice[J].Mol Cell Biol, 2016, 36(11): 1628-1638.
[6]  Sen S, Langiewicz M, Jumaa H, et al. Deletion of serine/arginine-rich splicing factor 3 in hepatocytes predisposes to hepatocellular carcinoma in mice[J]. Hepatology, 2015, 61(1): 171-183. 
[7] Elizalde M, Urtasun R, Azkona M, et al. Splicing regulator SLU7 is essential for maintaining liver homeostasis[J]. J Clin Invest, 2014, 124(7): 2909-2920. 
[8]  王超玄, 侯宇, 陈哲, 等. 肝脏特异性DEK基因敲除小鼠模型的制备及鉴定[J]. 中国临床解剖学杂志, 2018, 36(4): 397-407.
[9] Su LX, Pan P, Wang XT, et al.Vimentin modulates apoptosis and inflammatory cytokine release by a human monocytic cell line (THP-1) in response to lipopolysaccharides in vitro[J]. Chin Med J (Engl), 2019, 132(11): 1336-1343.
[10] Tulotta C, Lefley DV, Freeman K, et al. Endogenous production of IL1B by breast cancer cells drives metastasis and colonization of the bone microenvironment[J]. Clin Cancer Res, 2019, 25(9): 2769-2782.

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