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ABSTRACT: This study investigated the process of PCV2-induced apoptosis and the effect of PCV2 inoculation on calcium homeostasis in piglet lymphocytes in vitro. PCV2-inoculated lymphocytes exhibited chromatin condensation, chromatin segregation, the appearance of membrane-enclosed apoptotic bodies, and DNA fragmentation. Moreover, the proportion of apoptotic cells increased significantly in PCV2-inoculated lymphocytes compared with controls. These results demonstrate that PCV2 induces lymphocyte apoptosis. Some evidence suggests that an alteration in the intracellular free Ca(2+) concentration ([Ca(2+)]i) could cause apoptosis. We measured elevated [Ca(2+)]i in PCV2-inoculated lymphocytes for 12 or 24h compared with controls. Our results support that PCV2-induced apoptosis may be relative to [Ca(2+)]i. In addition, calmodulin (CaM) was increased in PCV2-inoculated lymphocytes for 12h compared with controls. The amount of CaM-dependent protein kinase II (CaMKII) did not change with PCV2 inoculation. We infer that the increased [Ca(2+)]i can bind CaM protein, but functions independently of CaMKII. Inositol 1,4,5-trisphosphate receptor (IP3R)-1 mRNA expression increased with PCV2 inoculation, whereas plasma Ca(2+)-ATP4 mRNA expression decreased. A decreased Ca(2+)-ATP4 level may inhibit Ca(2+) efflux, and the increased IP3R-1 may trigger Ca(2+) release from the endoplasmic reticulum. Both of these changes may contribute to increased [Ca(2+)]i.
Research in Veterinary Science 04/2012; 93(3):1525-30. · 1.77 Impact Factor