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Toxoplasma gondii ROP17 promotes autophagy via the Bcl-2-Beclin 1 pathway
M. Guo, J. Sun, W. T. Wang, H. Y. Liu, Y. H. Liu, K. R. Qin, J. R. Hu, X. Y. Li, H. L. Liu, W. Wang, Z. Y. Chen, C. F. Wang, H. L. Wang
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články
ProQuest Central od 2004-01-01 do Před 3 měsíci
Health & Medicine (ProQuest) od 2004-01-01 do Před 3 měsíci
Public Health Database (ProQuest) od 2004-01-01 do Před 3 měsíci
ROAD: Directory of Open Access Scholarly Resources od 1982
Odkazy
PubMed
34180401
DOI
10.14411/fp.2021.016
Knihovny.cz E-zdroje
- MeSH
- autofagie genetika MeSH
- beclin 1 metabolismus MeSH
- faktory virulence genetika metabolismus MeSH
- HEK293 buňky MeSH
- lidé MeSH
- myši MeSH
- protoonkogenní proteiny c-bcl-2 metabolismus MeSH
- protozoální proteiny genetika metabolismus MeSH
- Toxoplasma genetika fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
The apicomplexan Toxoplasma gondii (Nicolle et Manceaux, 1908) secretes a group of serine/threonine kinases from rhoptries, which play vital roles in boosting intracellular infection. Toxoplasma gondii rhoptry organelle protein 17 (ROP17) is one of these important kinase proteins. Nevertheless, its function remains unclear. Here, we showed that ROP17 induced autophagy in vitro and in vivo. The autophagy of small intestine tissues of T. gondii tachyzoite (RH strain)-infected mice was detected by the immunohistochemistry staining of LC3B, Beclin 1 and P62. ROP17 overexpression augmented starvation-induced autophagy in HEK 293T cells as measured by MDC staining, transmission electron microscopy (TEM), fluorescence microscopy and Western blot analysis. Moreover, the interaction of ROP17 and Bcl-2 was confirmed using co-immunoprecipitation analysis, and the data demonstrated that ROP17 had an autophagic role dependent on the Beclin 1-Bcl-2 pathway, which was also revealed in an in vivo model through immunohistochemical staining. Pearson coefficient analysis showed that there existed strong positive correlations between the expression of ROP17 and LC3B, Beclin 1 and phosphorylation of Bcl-2, while strong negative correlations between the expression of ROP17 and p62 and Bcl-2. Collectively, our findings indicate that ROP17 plays a pivotal role in maintaining T. gondii proliferation in host cells via the promotion of autophagy-dependent survival.
Literatura
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- $a The apicomplexan Toxoplasma gondii (Nicolle et Manceaux, 1908) secretes a group of serine/threonine kinases from rhoptries, which play vital roles in boosting intracellular infection. Toxoplasma gondii rhoptry organelle protein 17 (ROP17) is one of these important kinase proteins. Nevertheless, its function remains unclear. Here, we showed that ROP17 induced autophagy in vitro and in vivo. The autophagy of small intestine tissues of T. gondii tachyzoite (RH strain)-infected mice was detected by the immunohistochemistry staining of LC3B, Beclin 1 and P62. ROP17 overexpression augmented starvation-induced autophagy in HEK 293T cells as measured by MDC staining, transmission electron microscopy (TEM), fluorescence microscopy and Western blot analysis. Moreover, the interaction of ROP17 and Bcl-2 was confirmed using co-immunoprecipitation analysis, and the data demonstrated that ROP17 had an autophagic role dependent on the Beclin 1-Bcl-2 pathway, which was also revealed in an in vivo model through immunohistochemical staining. Pearson coefficient analysis showed that there existed strong positive correlations between the expression of ROP17 and LC3B, Beclin 1 and phosphorylation of Bcl-2, while strong negative correlations between the expression of ROP17 and p62 and Bcl-2. Collectively, our findings indicate that ROP17 plays a pivotal role in maintaining T. gondii proliferation in host cells via the promotion of autophagy-dependent survival.
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