Ülfet Çetinkaya1, Armağan Caner2, Arzuv Charyyeva3, Meryem Şentürk4, Meryem Eren4. 1. Erciyes University Halil Bayraktar Vocational School of Health Services, HalilBayraktar Health Vocational College, Erciyes University, 38039, Kayseri, Turkey. ucetinkaya@erciyes.edu.tr. 2. Department of Biophysics, Faculty of Medicine, Erciyes University, Kayseri, Turkey. 3. Faculty of Science, Ostrava University Life Science Research Centre, Ostrava, Czech Republic. 4. Department of Biochemistry, Faculty of Veterinary Medicine, Erciyes University, Kayseri, Turkey.
Abstract
PURPOSE: Encephalitozoon intestinalis affects many physiological processes of host cells to survive, proliferate, and spread to different regions within the body. In this study, the effects of the parasite on host cell apoptosis and proliferation were investigated. METHODS: To determine the impact of the parasite on the host cell apoptosis, changes in the expression profile of genes were investigated with the qPCR array using the Human Apoptosis Panel in infected and non-infected macrophage cells. Also, the rate of apoptosis in the cells was determined by Giemsa staining method. Cell proliferation was determined by measuring the DNA concentration in infected and non-infected cells. RESULTS: The thirty-six of apoptosis-related genes were down-regulated, while 20 of apoptosis-related genes were up-regulated in infected cells compared to uninfected cells. However, there were no significant changes detected in 32 analyzed genes between infected and control groups. E. intestinalis was determined to decrease cell proliferation in U937 macrophage cells. Unexpectedly, Giemsa staining showed an increase in the rate of apoptosis in infected cells. CONCLUSION: Regulated genes after infection are involved in many different biological pathways and various components of the cell. This suggests that the parasite uses highly sophisticated ways to maintain the viability of the cell.
PURPOSE:Encephalitozoon intestinalis affects many physiological processes of host cells to survive, proliferate, and spread to different regions within the body. In this study, the effects of the parasite on host cell apoptosis and proliferation were investigated. METHODS: To determine the impact of the parasite on the host cell apoptosis, changes in the expression profile of genes were investigated with the qPCR array using the Human Apoptosis Panel in infected and non-infected macrophage cells. Also, the rate of apoptosis in the cells was determined by Giemsa staining method. Cell proliferation was determined by measuring the DNA concentration in infected and non-infected cells. RESULTS: The thirty-six of apoptosis-related genes were down-regulated, while 20 of apoptosis-related genes were up-regulated in infected cells compared to uninfected cells. However, there were no significant changes detected in 32 analyzed genes between infected and control groups. E. intestinalis was determined to decrease cell proliferation in U937 macrophage cells. Unexpectedly, Giemsa staining showed an increase in the rate of apoptosis in infected cells. CONCLUSION: Regulated genes after infection are involved in many different biological pathways and various components of the cell. This suggests that the parasite uses highly sophisticated ways to maintain the viability of the cell.
Entities:
Keywords:
Apoptosis; Cell proliferation; Gene; Human macrophage; Microsporidia; Parasites
Authors: Clemencia Ovalle-Bracho; Carlos Franco-Muñoz; Diana Londoño-Barbosa; Daniel Restrepo-Montoya; Carlos Clavijo-Ramírez Journal: PLoS One Date: 2015-06-08 Impact factor: 3.240