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p53 signaling modulation of cell cycle arrest and viral replication in porcine circovirus type 2 infection cells.
Vet Res. 2016 11 29; 47(1):120.VR

Abstract

Porcine circovirus type 2 (PCV2) is a ubiquitous pathogen in the swine industry worldwide. Previous studies have shown that PCV2 infection induces host cell apoptosis through up-regulation of p53. To further identify the regulatory roles of p53 signaling in the process of PCV2 infection, we established p53 gene knockout PK15 cell lines using the genomic editor tool CRISPR/Cas9, and further investigated the roles of p53 in modulating the cell cycle and viral replication in this study. The results show that PCV2 infection induced obvious S phase accumulation in wild-type PK15 cells and a compromised S phase accumulation in the p53 gene mutation cells (813PK15 p53m/m), but did not induce obvious S phase accumulation in the p53 gene knockout cells (148PK15 p53-/-) compared with the respective mock infection. PCV2 infection activated p53 signaling, up-regulated the expression of p21, Cyclin E, and down-regulated Cyclin A, CDK2. In p53 deficient cells, however, PCV2-induced changes in Cyclin A, CDK2, and Cyclin E were efficiently reversed to the basal levels. Detection of PCV2 replication showed decreased viral ORF1 genomic DNA in p53 deficient cells (148PK15 p533-/-) and p53 mutated cells (813PK15 p53m/m) compared with p53 wild-type cells after different synchronization treatment. Furthermore, PCV2 viral genomic DNA and Cap protein levels were higher in the cells released from S phase synchronized cells than in the cells released from the G0/G1 phase or G2/M phase-synchronized, or asynchronous cells after 18 h post-infection. Taken together, this study demonstrates that PCV2 infection induces S phase accumulation to favor viral replication in host cells through activation of the p53 pathway.

Authors+Show Affiliations

College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China. yonghuang@nwsuaf.edu.cn.College of Veterinary Medicine, Northwest A&F University, 22 Xinong Rd, Yangling, Shaanxi, 712100, People's Republic of China. dwtong@nwsuaf.edu.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27899159

Citation

Xu, Dan, et al. "P53 Signaling Modulation of Cell Cycle Arrest and Viral Replication in Porcine Circovirus Type 2 Infection Cells." Veterinary Research, vol. 47, no. 1, 2016, p. 120.
Xu D, Du Q, Han C, et al. P53 signaling modulation of cell cycle arrest and viral replication in porcine circovirus type 2 infection cells. Vet Res. 2016;47(1):120.
Xu, D., Du, Q., Han, C., Wang, Z., Zhang, X., Wang, T., Zhao, X., Huang, Y., & Tong, D. (2016). P53 signaling modulation of cell cycle arrest and viral replication in porcine circovirus type 2 infection cells. Veterinary Research, 47(1), 120.
Xu D, et al. P53 Signaling Modulation of Cell Cycle Arrest and Viral Replication in Porcine Circovirus Type 2 Infection Cells. Vet Res. 2016 11 29;47(1):120. PubMed PMID: 27899159.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - p53 signaling modulation of cell cycle arrest and viral replication in porcine circovirus type 2 infection cells. AU - Xu,Dan, AU - Du,Qian, AU - Han,Cong, AU - Wang,Zengguo, AU - Zhang,Xiujuan, AU - Wang,Tongtong, AU - Zhao,Xiaomin, AU - Huang,Yong, AU - Tong,Dewen, Y1 - 2016/11/29/ PY - 2016/05/12/received PY - 2016/09/20/accepted PY - 2016/12/1/entrez PY - 2016/12/3/pubmed PY - 2017/10/11/medline SP - 120 EP - 120 JF - Veterinary research JO - Vet. Res. VL - 47 IS - 1 N2 - Porcine circovirus type 2 (PCV2) is a ubiquitous pathogen in the swine industry worldwide. Previous studies have shown that PCV2 infection induces host cell apoptosis through up-regulation of p53. To further identify the regulatory roles of p53 signaling in the process of PCV2 infection, we established p53 gene knockout PK15 cell lines using the genomic editor tool CRISPR/Cas9, and further investigated the roles of p53 in modulating the cell cycle and viral replication in this study. The results show that PCV2 infection induced obvious S phase accumulation in wild-type PK15 cells and a compromised S phase accumulation in the p53 gene mutation cells (813PK15 p53m/m), but did not induce obvious S phase accumulation in the p53 gene knockout cells (148PK15 p53-/-) compared with the respective mock infection. PCV2 infection activated p53 signaling, up-regulated the expression of p21, Cyclin E, and down-regulated Cyclin A, CDK2. In p53 deficient cells, however, PCV2-induced changes in Cyclin A, CDK2, and Cyclin E were efficiently reversed to the basal levels. Detection of PCV2 replication showed decreased viral ORF1 genomic DNA in p53 deficient cells (148PK15 p533-/-) and p53 mutated cells (813PK15 p53m/m) compared with p53 wild-type cells after different synchronization treatment. Furthermore, PCV2 viral genomic DNA and Cap protein levels were higher in the cells released from S phase synchronized cells than in the cells released from the G0/G1 phase or G2/M phase-synchronized, or asynchronous cells after 18 h post-infection. Taken together, this study demonstrates that PCV2 infection induces S phase accumulation to favor viral replication in host cells through activation of the p53 pathway. SN - 1297-9716 UR - https://www.unboundmedicine.com/medline/citation/27899159/p53_signaling_modulation_of_cell_cycle_arrest_and_viral_replication_in_porcine_circovirus_type_2_infection_cells_ L2 - https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-016-0403-4 DB - PRIME DP - Unbound Medicine ER -