Metabolomic and Proteomic Profiling of Porcine Intestinal Epithelial Cells Infected with Porcine Epidemic Diarrhea Virus

被引:7
|
作者
Wang, Haifei [1 ]
Hui, Peng [1 ]
Uemoto, Yoshinobu [2 ]
Ding, Yueyun [3 ]
Yin, Zongjun [3 ]
Bao, Wenbin [1 ,4 ]
机构
[1] Yangzhou Univ, Coll Anim Sci & Technol, Key Lab Anim Genet Breeding Reprod & Mol Design, Yangzhou 225009, Peoples R China
[2] Tohoku Univ, Grad Sch Agr Sci, Anim Breeding & Genet, Sendai 9808572, Japan
[3] Anhui Agr Univ, Coll Anim Sci & Technol, Hefei 230036, Peoples R China
[4] Yangzhou Univ, Joint Int Res Lab Agr & Agriprod Safety, Minist Educ China, Yangzhou 225009, Peoples R China
关键词
porcine epidemic diarrhea virus; metabolomics; proteomics; virus replication; COMPLEMENT; INHIBITION; EXPRESSION; ROLES;
D O I
10.3390/ijms24065071
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
Porcine epidemic diarrhea virus (PEDV) infection results in severe epidemic diarrhea and the death of suckling pigs. Although new knowledge about the pathogenesis of PEDV has been improved, alterations in metabolic processes and the functional regulators involved in PEDV infection with host cells remain largely unknow. To identify cellular metabolites and proteins related to PEDV pathogenesis, we synergistically investigated the metabolome and proteome profiles of PEDV-infected porcine intestinal epithelial cells by liquid chromatography tandem mass spectrometry and isobaric tags for relative and absolute quantification techniques. We identified 522 differential metabolites in positive and negative ion modes and 295 differentially expressed proteins after PEDV infection. Pathways of cysteine and methionine metabolism, glycine, serine and threonine metabolism, and mineral absorption were significantly enriched by differential metabolites and differentially expressed proteins. The betaine-homocysteine S-methyltransferase (BHMT) was indicated as a potential regulator involved in these metabolic processes. We then knocked down the BHMT gene and observed that down-expression of BHMT obviously decreased copy numbers of PEDV and virus titers (p < 0.01). Our findings provide new insights into the metabolic and proteomic profiles in PEDV-infected host cells and contribute to our further understanding of PEDV pathogenesis.
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页数:12
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