Journal article
Authors list: Velasquez, Zahady D.; Lopez-Osorio, Sara; Pervizaj-Oruqaj, Learta; Herold, Susanne; Hermosilla, Carlos; Taubert, Anja
Publication year: 2020
Pages: 2563-2577
Journal: Parasitology Research
Volume number: 119
Issue number: 8
ISSN: 0932-0113
eISSN: 1432-1955
Open access status: Hybrid
DOI Link: https://doi.org/10.1007/s00436-020-06744-x
Publisher: Springer
Abstract:
Besnoitia besnoitiis an important obligate intracellular parasite of cattle which primarily infects host endothelial cells of blood vessels during the acute phase of infection. Similar to the closely related parasiteToxoplasma gondii,B. besnoitihas fast proliferating properties leading to rapid host cell lysis within 24-30 h p.i. in vitro. Some apicomplexan parasites were demonstrated to modulate the host cellular cell cycle to successfully perform their intracellular development. As such, we recently demonstrated thatT. gondiitachyzoites induce G2/M arrest accompanied by chromosome missegregation, cell spindle alteration, formation of supernumerary centrosomes, and cytokinesis impairment when infecting primary bovine umbilical vein endothelial cells (BUVEC). Here, we follow a comparative approach by using the same host endothelial cell system forB. besnoitiinfections. The current data showed that-in terms of host cell cycle modulation-infections of BUVEC byB. besnoititachyzoites indeed differ significantly from those byT. gondii. As such, cyclin expression patterns demonstrated a significant upregulation of cyclin E1 inB. besnoiti-infected BUVEC, thereby indicating parasite-driven host cell stasis at G1-to-S phase transition. In line, the mitotic phase of host cell cycle was not influenced since alterations of chromosome segregation, mitotic spindle formation, and cytokinesis were not observed. In contrast to respectiveT. gondii-related data, we furthermore found a significant upregulation of histone H3 (S10) phosphorylation inB. besnoiti-infected BUVEC, thereby indicating enhanced chromosome condensation to occur in these cells. In line to altered G1/S-transition, we here additionally showed that subcellular abundance of proliferating cell nuclear antigen (PCNA), a marker for G1 and S phase sub-stages, was affected byB. besnoitisince infected cells showed increased nuclear PCNA levels when compared with that of control cells.
Citation Styles
Harvard Citation style: Velasquez, Z., Lopez-Osorio, S., Pervizaj-Oruqaj, L., Herold, S., Hermosilla, C. and Taubert, A. (2020) Besnoitia besnoiti-driven endothelial host cell cycle alteration, Parasitology Research, 119(8), pp. 2563-2577. https://doi.org/10.1007/s00436-020-06744-x
APA Citation style: Velasquez, Z., Lopez-Osorio, S., Pervizaj-Oruqaj, L., Herold, S., Hermosilla, C., & Taubert, A. (2020). Besnoitia besnoiti-driven endothelial host cell cycle alteration. Parasitology Research. 119(8), 2563-2577. https://doi.org/10.1007/s00436-020-06744-x
Keywords
Apicomplexan parasites; COCCIDIA; FORCE GENERATION; HISTONE H3 PHOSPHORYLATION; Histone H3 S10; S-PHASE; SUBUNIT; TOXOPLASMA-GONDII