Expression and role of CCAAT enhancer binding protein β mRNA, microRNA-369-3p and rno-Rmdn2_0006 of hepatocytes during the rat liver regeneration initiation

XU Cun-Shuan

doi:10.16098/j.issn.0529-1356.2021.06.011

PDF(847 KB)

Acta Anatomica Sinica ›› 2021, Vol. 52 ›› Issue (6) : 913-916. DOI: 10.16098/j.issn.0529-1356.2021.06.011

Liver regeneration and cell cycle control

Expression and role of CCAAT enhancer binding protein β mRNA, microRNA-369-3p and rno-Rmdn2_0006 of hepatocytes during the rat liver regeneration initiation

BAI Ge^{1, 2} WANG Zi-hui^{1, 2} SONG Ya-ping^{1, 2} ZANG Xia-yan^{1, 2} LI Ya-fei^{1, 2}YE Bing-yu^{1, 2} ZHAO Zhi-hu^3*XU Cun-shuan ^{1, 2*}

Author information +

History +

Abstract

Objective To explore the pathways and patterns which CCAAT/enhancer binding protein β(CEBPβ) mRNA, miR-369-3p and rno-Rmdn2_0006 regulate the hepatocytes in G0 phase and G1 phase during rat liver regeneration (LR). Methods The rat 2/3 partial hepatectomy (PH) model was prepared as described by Higgins, the hepatocytes of rat liver right lobes were isolated in 9∶00-11∶00 am according to the method of Smedsrod et al, the large-scale quantitative detection of competitive endogenous RNA(ceRNAs) was processed by the high-throughput biotechnology, the interaction network of ceRNAs was constructed by Cytoscape 3.2 software, and the correlation in expression and role of ceRNAs was analyzed by ceRNA comprehensive analysis. Results It was found that at 0 hour and 6 hour after PH, the ratio value of CEBPβ mRNA showed 1.11±0.11 and 2.57±0.10, miR-136-3p displayed 0.70±0.22 and 0.28±0.03, rno-Rmdn2_0006 indicated 1.26±0.34 and 2.62±0.70. The G0 phase-related genes promoted by CEBPβ were following, the growth arrest and DNA damage inducible beta (GADD45β) 0.12±0.09 and 2.50±0.44, the cyclin dependent kinase inhibitor 1A(CDKN1A）0.39±0.07 and 0.93±0.15, but the G0 phase-related genes inbibited by CEBPβ were following, the cyclin dependent kinase 2 associated protein 2 (CDK2AP2) 2.55±0.42 and 0.74±0.11, the signal transducer and activator of transcription 1 (STAT1) 2.57±0.13 and 1.32±0.13. The G1 phase-related genes promoted by CEBPβ were following, the ETS variant transcription factor 6 (ETV6) 0.77±0.05 and 2.22±0.68, the hemoglobin oxygenase 1 (HMOX1) 1.05±0.21 and 4.57±0.88, the mitogen-activated protein kinase 14 (MAPK14) 1.01±0.15 and 2.01±0.32, the thioredoxin interacting protein (TXNIP) 1.03±0.07 and 2.50±0.19, but the G1 phase-related gene nuclear factor erythroid 2 like 2 (NFE2L2) inbibited by CEBPβ 0.66±0.09 and 0.35±0.05. Conclusion CEBPβ mRNA is not up-regulated at 0 hour after PH, that is helpful for the expression of the G0 phase-related genes inbibited by CEBPβ and for the hepatocytes to be in G0 phase. On the contrary, the interaction of miR-369-3p and rno-Rmdn2_0006 leads to CEBPβ mRNA to bind with miR-369-3p, to CEBPβ being formed probablely, and to the expression of the G1 phase-related genes promoted by CEBPβ probablely, and to the hepatocytes being in G1 phase at 6 hours after PH.

Key words

Liver regeneration / Hepatocyte in G0 phase / / Hepatocyte in G1 phase / CCAAT/enhancer binding protein β / Competitive endogenous RNA comprehensive analysis / Biological hig-throughput detection / Rat

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

BAI Ge WANG Zi-hui SONG Ya-ping ZANG Xia-yan LI Ya-fei YE Bing-yu ZHAO Zhi-hu XU Cun-shuan. Expression and role of CCAAT enhancer binding protein β mRNA, microRNA-369-3p and rno-Rmdn2_0006 of hepatocytes during the rat liver regeneration initiation[J]. Acta Anatomica Sinica. 2021, 52(6): 913-916 https://doi.org/10.16098/j.issn.0529-1356.2021.06.011

References

［1］ Zimmermann A. Regulation of liver regeneration ［J］. Nephrol Dial Transplant, 2004, 19 （Suppl 4）:iv6-10.

［2］ Zang XY, Wang ZH, Li YF, et al. Expression and role of CCAAT enhancer binding protein α mRNA, miR-144-3p and three kinds of circular RNAs of hepatocytes during the rat liver regeneration initiation ［J］. Acta Anatomica Sinica, 2021, 52(6):901908. (in Chinese)

臧夏炎,王子慧,李亚霏,等.大鼠肝再生启动阶段CCAAT增强子结合蛋白α mRNA、miR-144-3p和3种环状RNA的表达和作用［J］.解剖学报,2021,52(6):901-908.

［3］ Higgins GM, Anderson RM. Experimental pathology of the liver: restoration of the liver of the white rat following partial surgical removal ［J］. Arch Pathol, 1931, 12:186-202.

［4］ Xia YCh, Cheng XM, Yao L, et al. Hepatitis B virus deregulates the cell cycle to promote viral replication and a oremalignant phenotype ［J］.J Virol, 2018, 92(19):e00722-e00728.

［5］ Aguilar-Morante D, Cortes-Canteli M, Sanz-Sancristobal M, et al. Decreased CCAAT/enhancer binding protein β expression inhibits the growth of glioblastoma cells ［J］. Neuroscience, 2011, 176:110-119.

［6］ Saghaeian Jazi M, Samaei NM, Mowla SJ, et al. SOX2OT knockdown derived changes in mitotic regulatory gene network of cancer cells ［J］. Cancer Cell Int, 2018, 18:129.

［7］ Liu Q, Liu X, Gao JL, et al. Overexpression of DOC-1R inhibits cell cycle G1/S transition by repressing CDK2 expression and activation ［J］. Int J Biol Sci, 2013, 9(6):541-549.

［8］ Kageyama K, Sugiyama A, Murasawa S, et al. Aphidicolin inhibits cell proliferation via the p53-GADD45β pathway in AtT-20 cells ［J］. Endocr J, 2015, 62(7):645-654.

［9］ Sánchez-Abarca LI, Gutierrez-Cosio S, Santamaría C, et al. Immunomodulatory effect of 5-azacytidine (5-azaC): potential role in the transplantation setting ［J］. Blood, 2010, 115(1):107-121.

［10］ Kurakazu Ⅰ, Akasaki Y, Hayashida M, et al. FOXO1 transcription factor regulates chondrogenic differentiation through transforming growth factor β1 signaling ［J］. J Biol Chem, 2019, 294(46):17555-17569.

［11］ Zhang X, Qin Y, Pan Z, et al. Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells ［J］. Biomolecules, 2019, 9(8):302.

［12］ Chen JY, Wang HH, Wang J, et al. STAT1 inhibits human hepatocellular carcinoma cell growth through induction of p53 and Fbxw7 ［J］. Cancer Cell Int, 2015, 15:111.

［13］ Han SH, Jeon JH, Ju HR, et al. VDUP1 upregulated by TGF-beta1 and 1,25-dihydorxyvitamin D3 inhibits tumor cell growth by blocking cell-cycle progression ［J］. Oncogene, 2003, 22(26):4035-4046.

［14］ Xie M, Xie RY, Xie S, et al. Thioredoxin interacting protein (TXNIP) acts as a tumor suppressor in human prostate cancer ［J］. Cell Biol Int, 2020, 44（10）:2094-2106.

［15］ Yamaguchi F, Hirata Y, Akram H, et al. FOXO/TXNIP pathway is involved in the suppression of hepatocellular carcinoma growth by glutamate antagonist MK-801 ［J］. BMC Cancer, 2013, 13:468.

［16］ Xu LL, Feng XF, Hao XY, et al. CircSETD3 (Hsa_circ_0000567) acts as a sponge for microRNA-421 inhibiting hepatocellular carcinoma growth ［J］. J Exp Clin Cancer Res, 2019, 38(1):98.

［17］ Lin DW, Chung BP, Kaiser P. S-adenosylmethionine limitation induces p38 mitogen-activated protein kinase and triggers cell cycle arrest in G1 ［J］. J Cell Sci, 2014, 127(Pt 1):50-59.

［18］ Schick N, Oakeley EJ, Hynes NE, et al. TEL/ETV6 is a signal transducer and activator of transcription 3 (Stat3)-induced repressor of Stat3 activity ［J］.J Biol Chem, 2004, 279(37):38787-38796.

［19］ Nishimura N, Furukawa Y, Sutheesophon K, et al. Suppression of ARG kinase activity by STI571 induces cell cycle arrest through up-regulation of CDK inhibitor p18/INK4c ［J］. Oncogene, 2003, 22(26):4074-4082.

［20］ Zhou Z, Ma D, Liu P, et al. Deletion of HO-1 blocks development of B lymphocytes in mice ［J］. Cell Signal, 2019, 63:109378.

［21］ Peyton KJ, Liu XM, Yu Y, et al. Glutaminase-1 stimulates the proliferation, migration, and survival of human endothelial cells ［J］.Biochem Pharmacol, 2018, 156:204-214.

［22］ K?hler UA, Kurinna S, Schwitter D, et al. Activated Nrf2 impairs liver regeneration in mice by activation of genes involved in cell-cycle control and apoptosis ［J］.Hepatology, 2014, 60(2):670-678.

［23］ Jee YH, Wang JH, Yue S, et al. mir-374-5p, mir-379-5p, and mir-503-5p regulate proliferation and hypertrophic differentiation of growth plate chondrocytes in male rats ［J］.Endocrinology, 2018,159(3):1469-1478.

［24］ Bing WD, Pang XY, Qu QX, et al. Simvastatin improves the homing of BMSCs via the PI3K/AKT/miR-9 pathway ［J］. J Cell Mol Med, 2016, 20（5）:949-961.