ArticleParasites & vectors2017
A mechanistic study of Toxoplasma gondii ROP18 inhibiting differentiation of C17.2 neural stem cells.
Article in Parasites & vectors, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Mechanisms of parasite-mediated disruption of brain vessels.FEBS letters · 2026Review
- Changes in the Proliferation of the Neural Progenitor Cells of Adult Mice Chronically Infected withMicroorganisms · 2023Article
- Wnt signaling in colorectal cancer: pathogenic role and therapeutic target.Molecular cancer · 2022Review
- TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection.Parasites & vectors · 2020Article
- Transcriptome Profiling ofMicroorganisms · 2020Article
- ROP18-Mediated Transcriptional Reprogramming of HEK293T Cell Reveals New Roles of ROP18 in the Interplay BetweenFrontiers in cellular and infection microbiology · 2020Article
- Unexpected encounter of the parasitic kind.World journal of stem cells · 2019Review
- Toxoplasma gondii ROP17 inhibits the innate immune response of HEK293T cells to promote its survival.Parasitology research · 2019Article
- Tryptophan-kynurenine pathway attenuates β-catenin-dependent pro-parasitic role of STING-TICAM2-IRF3-IDO1 signalosome in Toxoplasma gondii infection.Cell death & disease · 2019Article
- Protein targets of thiazolidinone derivatives in Toxoplasma gondii and insights into their binding to ROP18.BMC genomics · 2018Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCongenital infection of Toxoplasma gondii is an important factor causing birth defects. The neural stem cells (NSCs) are found to be one of the target cells for the parasite during development of the brain. As a key virulence factor of the parasite that hijacks host cellular functions, ROP18 has been demonstrated to mediate the inhibition of host innate and adaptive immune responses through specific binding different host immunity related molecules. However, its pathogenic actions in NSCs remain elusive.
resultsIn the present study, ROP18 recombinant adenovirus (Ad-ROP18) was constructed and used to infect C17.2 NSCs. After 3d- or 5d-culture in differentiation medium, the differentiation of C17.2 NSCs and the activity of the Wnt/β-catenin signaling pathway were detected. The results showed that the protein level of βIII-tubulin, a marker of neurons, in the Ad-ROP18-transfected C17.2 NSCs was significantly decreased, indicating that the differentiation of C17.2 NSCs was inhibited by the ROP18. The β-catenin level in the Ad-ROP18-transfected C17.2 NSCs was found to be lower than that in the Ad group. Also, neurogenin1 (Ngn1) and neurogenin2 (Ngn2) were downregulated significantly (P < 0.05) in the Ad-ROP18-transfected C17.2 NSCs compared to the Ad group. Accordingly, the TOP flash/FOP flash dual-luciferase report system showed that the transfection of Ad-ROP18 decreased the Wnt/β-catenin pathway activity in the C17.2 NSCs.
conclusionsThe inhibition effect of the ROP18 from T. gondii (TgROP18) on the neuronal differentiation of C17.2 NSCs was at least partly mediated through inhibiting the activity of the Wnt/β-catenin signaling pathway, eventually resulting in the downregulation of Ngn1 and Ngn2. The findings help to better understand potential mechanisms of brain pathology induced by TgROP18.
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