| Literature DB >> 24092455 |
Juwar Doley1, Lakshya Veer Singh, G Ravi Kumar, Aditya Prasad Sahoo, Lovleen Saxena, Uttara Chaturvedi, Shikha Saxena, Rajiv Kumar, Prafull Kumar Singh, R S Rajmani, Lakshman Santra, S K Palia, S Tiwari, D R Harish, Arvind Kumar, G S Desai, Smita Gupta, Shishir K Gupta, A K Tiwari.
Abstract
The canine parvovirus type 2 (CPV-2) causes an acute disease in dogs. It has been found to induce cell cycle arrest and DNA damage leading to cellular lysis. In this paper, we evaluated the apoptotic potential of the "new CPV-2a" in MDCK cells and elucidated the mechanism of the induction of apoptosis. The exposure of MDCK cells to the virus was found to trigger apoptotic response. Apoptosis was confirmed by phosphatidylserine translocation, DNA fragmentation assays, and cell cycle analysis. Activation of caspases-3, -8, -9, and -12 and decrease in mitochondrial potential in CPV-2a-infected MDCK cells suggested that the CPV-2a-induced apoptosis is caspase dependent involving extrinsic, intrinsic, and endoplasmic reticulum pathways. Increase in p53 and Bax/Bcl2 ratio was also observed in CPV-2a-infected cells.Entities:
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Year: 2013 PMID： 24092455 DOI： 10.1007/s12010-013-0538-y
Source DB: PubMed Journal: Appl Biochem Biotechnol ISSN： 0273-2289 Impact factor: 2.926