Publication: Effect of praziquantel on schistosoma mekongi proteome and phosphoproteome
Issued Date
2020-06-01
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ISSN
20760817
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2-s2.0-85085594761
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Mahidol University
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SCOPUS
Bibliographic Citation
Pathogens. Vol.9, No.6 (2020)
Suggested Citation
Peerut Chienwichai, Sumate Ampawong, Poom Adisakwattana, Tipparat Thiangtrongjit, Yanin Limpanont, Phiraphol Chusongsang, Yupa Chusongsang, Onrapak Reamtong Effect of praziquantel on schistosoma mekongi proteome and phosphoproteome. Pathogens. Vol.9, No.6 (2020). doi:10.3390/pathogens9060417 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/57721
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Title
Effect of praziquantel on schistosoma mekongi proteome and phosphoproteome
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Abstract
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Schistosoma mekongi causes schistosomiasis in southeast Asia, against which praziquantel (PZQ) is the only treatment option. PZQ resistance has been reported, thus increasing the requirement to understand mechanism of PZQ. Herein, this study aimed to assess differences in proteome and phosphoproteome of S. mekongi after PZQ treatment for elucidating its action. Furthermore, key kinases related to PZQ effects were predicted to identify alternative targets for novel drug development. Proteomes of S. mekongi were profiled after PZQ treatment at half maximal inhibitory concentration and compared with untreated worms. A total of 144 proteins were differentially expressed after treatment. In parallel, immunohistochemistry indicated a reduction of phosphorylation, with 43 phosphoproteins showing reduced phosphorylation, as identified by phosphoproteomic approach. Pathway analysis of mass spectrometric data showed that calcium homeostasis, worm antigen, and oxidative stress pathways were influenced by PZQ treatment. Interestingly, two novel mechanisms related to protein folding and proteolysis through endoplasmic reticulum-associated degradation pathways were indicated as a parasiticidal mechanism of PZQ. According to kinase–substrate predictions with bioinformatic tools, Src kinase was highlighted as the major kinase related to the alteration of phosphorylation by PZQ. Interfering with these pathways or applying Src kinase inhibitors could be alternative approaches for further antischistosomal drug development.