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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
PI3K signaling pathways modulated white spot syndrome virus (WSSV) replication in Procambarus clarkii
Huijing Zhang1, Xuemei Yao2, Yunfei Ding3
1School of Basic Medical Sciences, Binzhou Medical University, Yantai, 264003, Shandong, China; State Key Laboratory of Marine Resource Utilization in South China Sea, Hainan University, Haikou, 570228, Hainan, China.
Abstract:
The PI3K/AKT signaling pathway is commonly exploited to regulate viral replication and affect the fate of infected cells. In the present study, a PI3K-specific inhibitor (LY294002) was employed to pretreat crayfish to evaluate the effects of PI3K/AKT signaling pathway in WSSV replication. The results showed that the WSSV copy numbers in crayfish pretreated with LY294002 were significantly lower than those in Tris-HCl pretreatment crayfish on the sixth and tenth day after WSSV infection. In semigranular cells, the apoptosis rates were up-regulated on the third day post-WSSV infection, and a significantly lower proportion of apoptosis cells were observed in LY294002-pretreatment group. The expression level of Bax, Bax inhibitor-1 and lectin mRNA in haemocytes of crayfish were increased after WSSV infection. After the secondary stimulation with Tris-HCl, the Bax expression level in LY294002-pretreatment crayfish was significantly higher than that of crayfish pretreated with Tris-HCl on the third or sixth day, but the Toll and lectin mRNA expression decreased significantly on the third, sixth and tenth day. The Bax mRNA expression levels in LY294002-WSSV group were significantly higher than those in Tris-HCl-WSSV group on the third and tenth day. The Bax inhibitor-1 mRNA expression levels in LY294002-WSSV group were significantly lower than those in Tris-HCl-WSSV crayfish on the third day. These results together indicated that the hosts PI3K/AKT signaling pathway play positive roles in WSSV replication through the balance between host cell apoptois and innate immune responses. This information is helpful to further understand the role of PI3K/AKT signaling pathway on WSSV replication in Decapoda crustaceans.
Insights
The PI3K/AKT pathway promotes WSSV replication in crayfish by balancing apoptosis and immune responses. Inhibiting this pathway reduces viral load and alters immune gene expression, offering insights into crustacean antiviral strategies.
Area of Science:
- Crustacean immunology
- Molecular biology
- Virology
Background:
- The Phosphoinositide 3-kinase/Protein kinase B (PI3K/AKT) signaling pathway is crucial for cellular processes, including viral replication and host cell fate.
- White Spot Syndrome Virus (WSSV) is a significant pathogen affecting Decapoda crustaceans, causing substantial economic losses in aquaculture.
Purpose of the Study:
- To investigate the role of the PI3K/AKT signaling pathway in WSSV replication in crayfish.
- To evaluate the impact of a PI3K-specific inhibitor on WSSV load, host cell apoptosis, and immune gene expression.
Main Methods:
- Crayfish were pretreated with a PI3K-specific inhibitor (LY294002) or a control (Tris-HCl) before WSSV infection.
- WSSV copy numbers were quantified using qPCR.
- Apoptosis rates in semigranular cells were assessed.
- The expression levels of immune-related genes (Bax, Bax inhibitor-1, lectin, Toll) were analyzed using RT-qPCR.
Main Results:
- LY294002 pretreatment significantly reduced WSSV copy numbers on days 6 and 10 post-infection.
- Inhibition of PI3K/AKT signaling led to a lower proportion of apoptotic cells in WSSV-infected crayfish.
- WSSV infection upregulated Bax, Bax inhibitor-1, and lectin mRNA. LY294002 treatment altered the expression of these genes and Toll mRNA.
Conclusions:
- The host PI3K/AKT signaling pathway plays a positive role in WSSV replication in crayfish.
- This pathway influences WSSV replication by modulating the balance between host cell apoptosis and innate immune responses.
- Targeting the PI3K/AKT pathway presents a potential strategy for managing WSSV infections in crustaceans.
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