ArticleParasitology research2016
Toxoplasma gondii ROP18: potential to manipulate host cell mitochondrial apoptosis.
Article in Parasitology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Toxoplasma gondii ROP18 inhibits human glioblastoma cell apoptosis through a mitochondrial pathway by targeting host cell P2X1.Parasites & vectors · 2019Article
- Strategies Developed byFrontiers in microbiology · 2019Review
- Article
- Genome-Wide Bimolecular Fluorescence Complementation-Based Proteomic Analysis ofFrontiers in immunology · 2018Article
- A Human Proteome Array Approach to Identifying Key Host Proteins Targeted byMolecular & cellular proteomics : MCP · 2017Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toxoplasma gondii is an obligate intracellular parasite that may manipulate host cell mitochondrial apoptosis pathways. In our experiment, 293T cells were transfected with the p3×FLAG-CMV-Myc-ROP18 vector and expressed the ROP18-Myc fusion protein. Cell apoptosis was induced by 0.5 μg/mL actinomycin D (ActD) and was detected by Annexin V-FITC/PI assay. The cell mitochondrial membrane potential was determined by JC-1. Cytochrome c (Cyto-c) from mitochondria and the cytoplasm was measured by Western blot. The Bcl-2 and Bax coding gene expression levels were detected by real-time PCR. We found, in vitro, that T. gondii ROP18 significantly suppressed 293T cell apoptosis induced by ActD and maintained mitochondrial membrane potential and integrity, thereby preventing the release of Cyto-c from mitochondria into the cytoplasm. The ratio of Bcl-2/Bax in ROP18-overexpressing cells was significantly higher than that of the negative control. Therefore, we speculate that ROP18 could suppress host cell apoptosis via the mitochondrial apoptosis pathway in vitro.
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