Human Parvovirus B19 Nonstructural Protein 1 Regulates GATA1 Expression via the Notch Signaling Pathway in K562 Cell Line

被引:3
作者
Zeng, Dongxin [1 ]
Zheng, Junwen [1 ]
Feng, Shuwen [1 ]
Fan, Panpan [1 ]
Zhao, Dongchi [1 ]
机构
[1] Wuhan Univ, Childrens Digital Hlth & Data Ctr, Dept Pediat, Zhongnan Hosp, Wuhan 430031, Hubei, Peoples R China
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2022年 / 27卷 / 09期
关键词
human parvovirus B19; nonstructural protein 1; GATA; Notch; hematopoietic cells; TRANSCRIPTION FACTORS; INFECTION; DIFFERENTIATION; GENE;
D O I
10.31083/j.fbl2709261
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Human parvovirus B19 (B19) infection can affect the hematopoietic arrest in fetus by hindering the differentiation and maturation of erythroid progenitor cells. B19 nonstructural protein 1 (NS1) has been shown to inhibit the differentiation of erythroid progenitor cells. The goal of this study is to explore the role of B19 NS1 in the regulation of GATA1 and Notch signaling pathway in hematopoietic cells. Methods: The B19 NS1 expression plasmid was reconstituted, and the possibility of NS1 regulating GATA1 and GATA2 expression modulated by Notch-Hes pathway was tested by qRT-PCR and western blot. Immunofluorescence assays were conducted to visualize pNS1 in K562 cells. Results: We demonstrate that B19 NS1 inhibited GATA1 and induced Hes1/Hes5, which is involved in the activation of Notch signaling pathway. Meanwhile, NS1 exhibited promoting effects on GATA2 expression. Activation of the Notch signaling pathway up-regulated its downstream transcriptional repressor family Hes, thereby inhibiting the expression of GATA gene in K562 cells. Conclusions: The results show that B19 NS1 protein negatively regulates GATA1 related nuclear transcription and may interfere with hematopoietic cell differentiation.
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页数:9
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共 35 条
[1]   Negative regulation of CD4 gene expression by a HES-1-c-Myb complex [J].
Allen, RD ;
Kim, HK ;
Sarafova, SD ;
Siu, G .
MOLECULAR AND CELLULAR BIOLOGY, 2001, 21 (09) :3071-3082
[2]   GATA-1 and c-myb crosstalk during red blood cell differentiation through GATA-1 binding sites in the c-myb promoter [J].
Bartunek, P ;
Králová, J ;
Blendinger, G ;
Dvorák, M ;
Zenke, M .
ONCOGENE, 2003, 22 (13) :1927-1935
[3]   Notch-1 induction, a novel activity of SV40 required for growth of SV40-transformed human mesothelial cells [J].
Bocchetta, M ;
Miele, L ;
Pass, HI ;
Carbone, M .
ONCOGENE, 2003, 22 (01) :81-89
[4]   Notch signalling: a simple pathway becomes complex [J].
Bray, Sarah J. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2006, 7 (09) :678-689
[5]   The small 11kDa nonstructural protein of human parvovirus B19 plays a key role in inducing apoptosis during B19 virus infection of primary erythroid progenitor cells [J].
Chen, Aaron Yun ;
Zhang, Elizabeth Yan ;
Guan, Wuxiang ;
Cheng, Fang ;
Kleiboeker, Steve ;
Yankee, Thomas M. ;
Qiu, Jianming .
BLOOD, 2010, 115 (05) :1070-1080
[6]  
Chen PM, 2008, INT J ONCOL, V32, P1335
[7]   A transgenic mouse model for non-immune hydrops fetalis induced by the NS1 gene of human parvovirus B19 [J].
Chisaka, H ;
Morita, E ;
Murata, K ;
Ishii, N ;
Yaegashi, N ;
Okamura, K ;
Sugamura, K .
JOURNAL OF GENERAL VIROLOGY, 2002, 83 :273-281
[8]   Parvovirus B19: Its Role in Chronic Arthritis [J].
Colmegna, Ines ;
Alberts-Grill, Noah .
RHEUMATIC DISEASE CLINICS OF NORTH AMERICA, 2009, 35 (01) :95-+
[9]   GATA factor mutations in hematologic disease [J].
Crispino, John D. ;
Horwitz, Marshall S. .
BLOOD, 2017, 129 (15) :2103-2110
[10]   New Insights of Human Parvovirus B19 in Modulating Erythroid Progenitor Cell Differentiation [J].
Feng, Shuwen ;
Zeng, Dongxin ;
Zheng, Junwen ;
Zhao, Dongchi .
VIRAL IMMUNOLOGY, 2020, 33 (08) :539-549