PCV2 trigger apoptosis of PK-15 cells through the PLC-IP3R-Ca2+
signaling pathway
Abstract
Phospholipase C (PLC) is a key enzyme in the cell membrane. PLC
hydrolyses phosphatidylinositol 4, 5-bisphosphate (PIP2) to
generateinositol 1,4, 5-triphosphate (IP3) and diacylglycerol (DAG) that
regulates a variety of cellular processes. Evidence indicates the
pivotal role of PLC and inositol 1,4,5-trisphosphate receptor(IP3R) in
influencing Ca2+ release from the endoplasmic reticulum(ER).At the same
time, the imbalance of Ca2+ will stimulate endoplasmic reticulum
stress(ERS), leading to cell apoptosis. Viral infection could triggers
host defense through apoptosis of the infected cells.However, it is not
clear how porcine circovirus type 2 (PCV2) induces apoptosis by
affecting Ca2+ homeostasis. We show here that PCV2 infection induces the
increased cytoplasmic Ca2+ level and apoptosis.We also found that the ER
swelling of PK-15 cells after viral infection by transmission electron
microscopy. Furthemore, the activation of PLC-IP3R-Ca2+ signaling
enhanced apoptosis in infected PK-15 cells. Taken together,our findings
suggest that PCV2 infection trigger ERS of PK-15 cells via the
PLC-IP3R-Ca2+ signaling pathway to promoted the release of intracellular
Ca2+, and led to cell apoptosis.